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Jnana Therapeutics Expands Leadership Team with Two Experienced Biopharmaceutical Executives – Yahoo Finance

Company appoints Nick Pullen, PhD, as Senior VP, Head of Biology and Brian Danieli as VP, Head of Finance & Operations

Jnana Therapeutics, a biotechnology company targeting the solute carrier (SLC) family of metabolite transporters to treat underserved diseases, today announced that it has expanded its leadership team with the appointment of two accomplished biopharmaceutical executives: Nick Pullen, PhD, as Senior Vice President, Head of Biology, and Brian Danieli as Vice President, Head of Finance and Operations. These new executives join Jnana at a significant time in the companys evolution as it advances its first SLC transporter-targeted therapies toward clinical development.

Nick Pullen, PhD, Senior Vice President, Head of Biology

"Nick is an experienced and passionate leader in drug discovery and development with deep knowledge in several therapeutic areas, including renal disease and inflammation, that are highly relevant to our R&D work with SLC transporters," said Joel Barrish, PhD, co-founder and Chief Scientific Officer of Jnana Therapeutics. "We are delighted to welcome Nick to our team and look forward to his contributions in building our research and development strategy and helping guide our lead programs toward the clinic."

In the role of Senior Vice President, Head of Biology, Dr. Nick Pullen will work to further leverage Jnanas RAPID platform to systematically target SLC transporters and develop novel small molecule drug candidates. Dr. Pullen is an experienced drug discovery and development leader with 20 years of experience and a proven track-record of therapeutic innovation across multiple disease areas. Before joining Jnana, he was Vice President, Integrative Sciences, Inflammation & Immunology, Cardiovascular & Fibrosis, at Bristol Myers Squibb and prior to this, he served as Executive Director, Inflammation & Immunology for Celgene. In both of these roles, Dr. Pullen was responsible for scientific and strategic leadership of externalized drug discovery programs applying novel technologies and scientific insights to the expansion of the Inflammation & Immunology portfolio as well as more broadly. Dr. Pullen brings extensive experience in Inflammation & Fibrosis, following a career at Pfizer which spanned more than 15 years and brought multiple development candidates to clinical evaluation and touched many disease areas including renal disease, IBD and NASH, a breadth of experience with significant pertinence to the emerging Jnana portfolio. Dr. Pullen received his PhD in biochemistry from the University of Southampton in the UK.

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"The Jnana team have made remarkable progress in the development of technologies that open up the therapeutic opportunity afforded by targeting the SLC gene family. I am thrilled to be joining Jnana at this exciting stage in the companys growth and to help them build a pipeline of small molecules targeting SLC transporters," said Dr. Pullen.

Brian Danieli, Vice President, Head of Finance & Operations

"Brians extensive finance background and expertise will be a critical addition to the organization," said Caroline Stark Beer, Jnanas Chief Business Officer. "Were very pleased to welcome Brian to Jnana and look forward to Brians financial and operational leadership as we enter a new stage of growth."

As the Head of Finance and Operations of Jnana Therapeutics, Brian Danieli will expand the companys finance and operations infrastructure to allow for growth to a clinical-stage drug developer. Mr. Danieli is an expert finance leader with more than 20 years of global experience with fast-growing biotechnology companies. He joins Jnana from Momenta Pharmaceuticals, where he led Financial Planning & Analysis. Previously, he served for more than 20 years in roles of increasing responsibility at Sanofi Genzyme. His most recent position at Sanofi Genzyme was Head of Finance for North America Rare Disease and Rare Blood Disorders, and he drove all aspects of strategic financial planning and operations for the North American region for two business units representing $2B in combined sales with over 500 employees and 12 products. In his roles at Sanofi Genzyme, Mr. Danieli spearheaded the integration of Bioverativ and Ablynx acquisitions, implemented financial modeling and assembled franchise performance metrics for investor audiences. Earlier in his career, he held financial positions at Blue Cross Blue Shield of Massachusetts and KPMG. He earned a BS in accounting from Boston College.

"I am eager to leverage my experience to support Jnanas evolution in the next stage of its business," said Mr. Danieli. "I see tremendous potential for Jnanas platform to bring innovation to a range of diseases, and I am excited to be part of a team that is committed to bring novel medicines to make a difference in the lives of patients."

About Jnana Therapeutics

Jnana Therapeutics is a biotechnology company focused on opening the solute carrier (SLC) family of metabolite transporters as a target class to develop transformational therapeutics. Jnana uses its RAPID platform, a proprietary, cell-based drug discovery approach, to systematically target SLC transporters and develop best-in-class therapies to treat a wide range of diseases, including immune-mediated, neurological and metabolite-dependent diseases. Headquartered in Boston, Jnana is founded by world-renowned scientists and backed by leading life science investors. For more information, please visit http://www.jnanatx.com and follow us on Twitter and on LinkedIn.

View source version on businesswire.com: https://www.businesswire.com/news/home/20210203005102/en/

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Kathryn MorrisThe Yates Networkkathryn@theyatesnetwork.com 914-204-6412

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Jnana Therapeutics Expands Leadership Team with Two Experienced Biopharmaceutical Executives - Yahoo Finance

Immunology

[Full text] Lipid Profile and IL-17A in Allergic Rhinitis: Correlation With Diseas | JAA – Dove Medical Press

Dina Sheha,1 Lobna El-Korashi,2 Amany M AbdAllah,3 Marwa M El Begermy,4 Doaa M Elzoghby,5 Amira Elmahdi1

1Department of Internal Medicine, Allergy and Clinical Immunology, Faculty of Medicine, Ain Shams University, Cairo, Egypt; 2Department of Medical Microbiology and Immunology, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 3Department of Family Medicine, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 4Department of Otorhinolaryngology, Faculty of Medicine, Ain Shams University, Cairo, Egypt; 5Department of Clinical Pathology, Faculty of Medicine, Ain Shams University, Cairo, Egypt

Correspondence: Dina ShehaFaculty of Medicine, Ain Shams University, El-Abbassia Street, Cairo, 11566, EgyptTel +20 1001525144Email DinaSheha@med.asu.edu.eg

Background: Recent data display the possible role of cytokines such as interleukin-10 (IL-10), IL-17 and IL-23 as a link between dyslipidemia and atopy; however, the relationship between dyslipidemia, allergic rhinitis (AR), and the underlying mechanisms involved is unclear.Purpose: To measure the lipid profile and IL-17A level in AR patients in comparison to healthy controls, and correlate serum lipid level with the severity of symptoms and quality of life (QoL) of AR patients.Patients and Methods: Peripheral blood samples were collected from AR patients (n=70) and a control group (n=80). Samples were analyzed for serum total IgE by ELISA, serum lipid profile, and IL-17A level by ELISA. Severity of AR symptoms was assessed by visual analogue scale (VAS) score and the rhinoconjunctivitis QoL questionnaire.Results: Serum lipid profile and level of IL-17A in AR patients were significantly higher in comparison to controls (P < 0.001). Positive correlations were found between total cholesterol (TC) and the severity of AR and QoL. IL-17A was positively correlated with triglyceride (TG) level and low-density lipoprotein cholesterol (LDL-C) (P=0.011, r=0.303; P=0.043, r=0.242, respectively). Additionally, IL-17A was negatively correlated with high-density lipoprotein cholesterol (HDL-C) level (P=0.036, r= 0.251). IL-17A was positively correlated with both age and VAS score with statistical significance (P=0.033, r=0.225; P=0.011, r=0.302, respectively).Conclusion: Dyslipidemia might play a potential role in the severity of AR symptoms and impairment of patients QoL. Highlighting this association might alert physicians to evaluate the lipid profile in AR patients for timely diagnosis and treatment of dyslipidemia in an attempt to improve disease control and improve QoL.

Keywords: allergic rhinitis, cholesterol, dyslipidemia, IgE, interleukin-17, quality of life

Allergic rhinitis (AR) is a symptomatic disorder induced by exposure of the nasal mucosa to diverse aeroallergens that is mediated through immunoglobulin E (IgE) hypersensitivity reactions. AR is characterized by four cardinal symptoms of watery rhinorrhea, nasal obstruction, nasal itching and sneezing.1 AR has a wide prevalence, it is estimated to affect 2030% of adults and up to 40% of pediatrics.2 AR is associated with multiple comorbid disorders, including asthma, conjunctivitis, eczema, rhinosinusitis, adenoid hypertrophy, obstructive sleep apnea, disordered sleep with consequent educational and behavioural effects. These associated comorbidities negatively correlate with the quality of life (QoL), and work performance.3

Dyslipidemia is a major risk for atherosclerosis and cardiovascular diseases especially coronary heart disease (CHD), and may play a major role earlier than other risk factors.4 Dyslipidemia modulates the immune response through the release of pro-inflammatory mediators, activation of immune cells (eg, B-cell, T-cells and dendritic cells),5 promoting polarization of T-helper 2 (Th-2) and Th17 and downregulating interleukin-10 (IL-10) cytokine synthesis.6 Th2 and Th17 release cytokines as IL6, IL-1, IL-4, and IL-17.7 Th2 immune response with an increased production of IL-4 and tumour necrosis factor- (TNF-) has been described in AR.8

IL-17 cytokine, produced by Th17 cells, plays a pivotal role in host defense reactions, inflammatory diseases and allergic responses.IL-17 belongs to a family of cytokines that includes six members of different homology and function: IL-l7 (also IL-17A) IL-17B, IL-17C, IL-17D and IL-17 E.9 The role of TNF- and IL-17 in the pathogenesis and regulation of inflammation in autoimmune diseases such as psoriasis has been described previously.10,11 Serum IL-17A level correlated significantly with clinical and inflammatory markers in patients with persistent moderate to severe AR evaluated during the pollen season. Moreover, studies suggest that serum IL-17A level correlates with symptom scores and with the number of peripheral blood eosinophils, suggesting that Th-17 cells may be involved in the chronic allergic reaction. Authors even proposed IL-17A as a new biomarker of disease progression and allergy.12 Research suggests a link between cholesterol and the adaptive immune system, as both have the same immunological pathways involving Th1 toTh2 switch, an increase in Th2 related IgG1 and IgE release, and elevation of pro-inflammatory Th2 cytokines release such as IL-4.13

Numerous research investigated the association between dyslipidemia and allergic diseases. Fessler et al14 demonstrated the relationship between total cholesterol (TC) level and atopy in children 617 years of age. Ouyang et al15 reported increased allergic sensitisation with elevated low-density lipoprotein cholesterol (LDL-C) level. Kusunoki et al16 demonstrated a positive association between TC and LDL-C levels and the allergic sensitization in school-aged children. Similarly, a meta-analysis of ten studies investigated the lipid profile of asthmatics and found higher levels of LDL and low level of high-density lipoprotein (HDL) in asthma patients in comparison to controls.17 Vinding et al18 found higher LDL and triglycerides (TG) were associated with asthma, airway obstruction and higher incidence of aeroallergen sensitization. Elevated HDL was associated with reduction of airway obstruction and lower risk of aeroallergen sensitization. To our knowledge, only a few studies have explored the association of abnormal serum lipids in AR patients and its effect on disease severity.

Since IL-17A could represent a link between AR and dyslipidemia, we aimed to investigate the possible relationship between AR, IL-17A level and dyslipidemia, and correlate level with the severity of AR and QoL of AR patients.

Seventy adult AR patients and 80 healthy volunteers as a control group were enrolled in the current casecontrol study, conducted from March 2019 to August 2019. AR patients were selected by systematic randomization from patients attending the allergy outpatient clinic at Ain Shams University, Cairo and Zagazig University, Zagazig, Egypt. Laboratory Techniques were performed in the Medical Microbiology and Immunology Department, Zagazig University, Zagazig, Egypt. Healthy controls were apparently healthy individuals who were recruited from relatives of patients attending the internal medicine outpatient clinic. They had no chronic diseases or allergic disorders, they were not on regular medications and had no complaints concerning mental or physical health.

AR was diagnosed according to the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines.19 Inclusion criteria were atopic adult AR with a positive family history of atopy and positive skin prick test (SPT) for at least one inhalant allergen. Patients with asthma, those on statin therapy, patients with acute illness like high-grade fever, first 2 weeks following surgery, non-allergic inflammatory nasal pathology, sleep disorders, diabetics, obese patients, hypothyroid, hypertensive patients, smokers and patients with autoimmune disorders were excluded from the study. No patients received systemic steroids or immunotherapy within 1 month of enrollment. An informed verbal consent was obtained from all participants. The research ethics committee of Zagazig University approved the study (IRB number 6222-25-6-2020) and the procedure outlined for the obtainment of verbal consent. The whole process was documented and the consent was conducted with an impartial witness after which the consent was transcribed. The study procedure complies with the country regulations about subjects data protection and maintaining their integrity, and the study was conducted in accordance with the declarations of Helsinki.

Detailed medical history of allergy was collected from each participant including family history of atopy. Clinical examination (ear, nose, throat and chest examination), and SPT to common aeroallergens were performed in the clinic. Venous blood samples for serum lipid profile, serum total IgE and serum level of IL-17A weredrawn from all participants.

The severity of AR was measured using the visual analogue scale (VAS) score for global assessment of severity of nasal and non-nasal symptoms. AR patients were asked to rate the combination of the nasal and non-nasal symptoms on a scale (010 cm) as follows:

Mild: 03; Moderate: 3.17; Severe: 7.110.19

QoL was assessed in the AR group by the RQLQ total score. The instrument has 28 items in seven domains (sleep, non-rhinoconjunctivitis symptoms, practical problems, nasal symptoms, eye symptoms, activity limitations, and emotional function). The overall RQLQ score is the mean of all 28 responses.19

Skin testing was performed on AR patients according to Bernstein et al.20 A panel for the most common locally encountered inhaled allergens was used including house dust mites, cockroach, cotton, molds mix, ragweed, mugwort, Chenopodium album, hay dust, pigeon feathers, dog hair, cat hair, rabbit hair. Allergen extracts of skin testing were locally prepared at Allergy and Immunology Unit, Department of Internal Medicine, Faculty of Medicine, Ain Shams University. Aqueous allergen extracts (1:100 wt/vol) preparation was done according to allergen extract preparation guidelines developed by the AAAAI/ACAAI/JCAAI and all aqueous allergen extracts were stored at 4 C.21

The maximum or mean diameter of the wheal to various allergens was read at 15 minutes. A wheal of 3mm or more in diameter was considered positive (indicating sensitization to the allergen).

Under complete aseptic conditions, 10mL of fasting venous blood was obtained by a clean venipuncture in the early morning from all participants after 912 hours of fasting. Patients were on regular average diet 3 days before sampling. The serum was separated by centrifugation (1000 g for 15 minutes) and divided into three tubes. Serum of one tube was immediately assayed for lipid profile (TC, TG, HDL-C and LDL-C), while the serum collected in the other tube was stored at 20C for subsequent assay of the serum total IgE, IL-17A concentrations. Hemolysed samples were discarded. Repeated freezing and thawing was avoided.

Serum TC, triglycerides and HDL-C were assayed on Microlab 300 Semi Automated Clinical Chemistry Analyzer supplied by EliTech clinical system (France,www.elitechgroup.cominfo@elitechgroup.com).

TC, TG and HDL-C were assayed by (homogenous for HDL-C) enzymatic colorimetric quantitative determination at wavelength (500, 500, and 600/700 nm respectively) using kits provided by Human diagnostics kit (Human Gesellschaft fr Biomedica und Diagnostica mbH Max-Planck-Ring 21.6 5205 Wiesbaden-Germany). LDL-C was calculated according to the Friedwald equation.22

Dyslipidemia was defined according to the American College of Cardiology/American Heart Association (ACC/AHA) Blood Cholesterol 2013 Guideline, as follows: hypercholesterolemia was defined as total cholesterol (TC) level greater than 200 mg/dL and/or LDL-C level greater than 100 mg/dL, hypertriglyceridemia as TG level greater than 150 mg/dL; and low HDL-C lower than 40 mg/dL in men and 50 mg/dL in women.23

Quantitative measurement of total IgE in the serum was done using a commercially available quantitative enzyme-linked Immunosorbent assay (ELISA) Kit supplied by Calbiotech Inc. (1935 Cordell Ct., El Cajon, CA 92020, USA) according to the manufacturers instructions, and the results were expressed in IU/mL.

Human IL17-A was measured by commercially available quantitative ELISA Kit supplied by Thermo Fisher Scientific (Bender Med Systems gmbH/Campus Vienna Biocenter 2/1030 Vienna, Austria) according to the manufacturers instructions and expressed in pg/mL.

Data analysis was performed using the software SPSS (Statistical Package for the Social Sciences) version 20 (SPSS Inc., Chicago, Illinois, USA). Quantitative variables were described using means and standard deviations. Categorical variables were described using absolute frequencies and to compare the proportion of categorical data, chi square test was used when appropriate. KolmogorovSmirnov (distribution-type) and Levene (homogeneity of variances) tests were used to verify assumptions for use in parametric tests. To compare the means of two groups, independent sample t-test was used. MannWhitney test was used to compare continuous variables between two groups when data were not normally distributed. Pearson correlation and Spearman rank correlation coefficients were used to assess the strength and direction of a linear relationship between two variables. The level of statistical significance was set at 5% (P<0.05). Highly significant difference was present if P0.001.

Descriptive data of the study groups are represented in Table 1. Patients and controls were matched regarding age and gender. The mean age of AR patients was 30.74 years ( 7.24) and controls were 32.85 years ( 7.5). Total IgE and IL17-A level were significantly higher in cases in comparison to controls (Table 1). Runny nose, sneezing, nasal obstruction, postnasal drip, itchy nose, cough and eye symptoms prevailed in 60%, 62.9%, 72.9%, 30%, 20%, 38.6% and 10% of the patients within AR group, respectively.

Table 1 Demographic and Laboratory Data Characteristics of the Study Groups

Associated allergic conjunctivitis and atopic dermatitis co-existed in 30% and 3% respectively of those patients (Table 1)

Levels of TC and LDL-C were statistically significantly higher in cases than controls. Mean SD of TC in cases and controls was 225,6562.91mg/dl and 187.9235.24mg/dl, respectively.

Regarding HDL_C, meanSD in cases was 47.255.36 mg/dl and in controls 49.834.29 mg/dl, showing statistically significantly lower levels in cases than controls. There was a non-significant difference in serum TG and very-low-density lipoprotein cholesterol (VLDL-C) between the two groups (P=0.79, P=0.175) (Table 2).

Table 2 Serum Lipid Profile of Study Subjects

AR patients had significantly increased risk of dyslipidemia by 6.27-fold (95% confidence interval (CI) of crude odds ratio (COR)=2.7114.51, P<0.001). Approximately 44% of the patients with AR had dyslipidemia versus 11.2% of the healthy controls.

Correlation studies were performed to assess the relationship between serum lipid profile and the severity of AR assessed by VAS (P=0.039, r=0.31) and RQLQ score (P=0.04, r=0.247). There was a positive correlation between IL-17A and TG and LDL-C levels (P=0.011, 0.043, respectively). IL-17A level was negatively correlated to HDL-C level (P=0.036), while no significant correlation was found for the other correlation studies listed in Table 3.

Table 3 Correlation Between Serum Lipid Profile and Different Study Parameters

There was a statistically significant correlation between IL-17A and both age and VAS score (p=0.033, r=0.225, 0=0.011, r=0.302; 95% CI; 0.078:0.486) and VAS score (95% CI; 0.078:0.486). On the other hand, there was a non-significant correlation between IL-17A and total IgE and RQLQ score (Table 4).

Table 4 Correlation Between IL-17A and All of Patients Age, VAS, RQLQ, and Total IgE

Serum lipid levels and their clinical implication in the management and monitoring of cardiovascular diseases or diabetic patients is well established.24,25 On the contrary, the role of dyslipidemia in AR is not fully elucidated.

The current casecontrol study aimed to investigate the possible relationship between AR, IL-17A level and dyslipidemia and correlate levels with the severity of AR and QoL of AR patients. We included 70 AR patients and 80 healthy controls, and found dyslipidemia in 44% of AR patients versus 11.2% of controls. Levels of TC and LDL-C were significantly higher in AR patients, while HDL-C was significantly lower. Similarly, recent studies have demonstrated a significant association between high serum lipid levels and AR.26,27 Additionally, Schfer et al investigated the effect of serum cholesterol on atopy and found that elevation of serum cholesterol is associated with an increased incidence of atopic diseases.28 Recent publications suggest the role of dyslipidemia in promoting atopic inflammation, through polarizing Th2 response.7,29 Another proposed theory is the cholesterol trafficking. Cholesterol is a critical microdomain of cell wall lipid rafts that plays an essential role in cell signaling. Changes in these cholesterol rafts trigger the toll-like receptor-signaling pathway of the innate immune reaction, which in turn aggravates the atopic inflammation.30

We report a positive correlation between TC levels and both VAS score, and RQLQ score. Ahmed et al in a recent Egyptian study reported similar results,29 which was also confirmed by regression analysis of Yon et al.31 TC and LDL-C were associated with the severity of AR high TC, which has been reported to increase allergen-specific IgE synthesis thus exacerbating allergic symptoms, which denotes a positive correlation between dyslipidemia and atopy.32 This could be attributed to the impact of dyslipidemia on the immune system where dyslipidemia induces a shift toward an immunologic Th2-oriented response and exacerbates allergic inflammation.26,33 Additionally, hypercholesterolemia is known for being pro-inflammatory, inducing the release of inflammatory cytokines30 and in turn aggravating the symptoms of AR.

We assume the poor QoL is due to the burden of increased AR severity, as well as the socioeconomic and financial burden of treatment costs, and the metabolic burden of dyslipidemia. The inflammatory nature of AR causes nasal obstruction, sleep difficulties, snoring, hypersomnolence, diminished work performance, and finally insomnia that all negatively impact the patients QoL.

Several studies have suggested that metabolic factors, such as dyslipidemia, are related to allergic diseases, but the related causal mechanisms remain elusive.3436 Hence we investigated the role of IL-17A as a link between AR and dyslipidemia, in order to explore one of the cytokines incriminated in the pathogenesis.

We found higher levels of IL-17A in AR patients compared to controls. Similarly, many studies declared this finding.3743 Moreover, other studies found higher IL-17A positive cells in peripheral blood and nasal mucosa of AR patients compared to healthy controls.44,45 It seems that Th17 cells may be involved in the process of neutrophil infiltration that occurs during the acute phase of allergic reaction.46 Besides, IL-17 induces allergen-specific Th2 cell activation, hence the production of serum IgE and eosinophil accumulation suggesting a regulatory role in Th2-allergic immune response.47

We report a positive correlation between IL-17A level and both TG and LDL-C levels, while IL-17A was negatively correlated to HDL-C level among AR patients. These findings are in line with.26 This could be explained by the fact that dyslipidemia causesTh2 and Th17 polarization and cytokines release as (IL-4, IL-17) with decreased production of IL-10. These cytokines disturbance is related to chronic inflammation that is common to both atopic predisposition and dyslipidemia6,46,48 Similarly, Vinding et al found that triglyceride levels were associated with increased risk of aeroallergen sensitization, which is one cause of AR.18

Furthermore, we found significant positive correlation between IL-17A and AR severity assessed by VAS score. IL-17 is a pro-inflammatory cytokine which in turn explains its role in increasing the severity of AR symptoms. This is consistent with many other studies.49 Also, Nieminen et al50 showed that serum IL-17A levels and allergen-induced IL-17A messenger RNA expression correlate with symptom severity, as assessed via a VAS score and symptom medication score, respectively. In addition, Lu et al51 reported significant correlations between AR symptoms and the expression of IL-17 in nasal mucosa and peripheral blood.

A study by Shahsavan et al52 found that patients with moderate to severe persistent AR demonstrated significantly greater IL-22 and IL-17A production than healthy controls, suggesting that the development of persistent AR is influenced by these cytokines. A correlation was found between IL-22 and IL-17A serum levels, along with the mean number of IL-22 and IL-17A positive cells in the nasal mucosa, and specific IgE levels, nasal eosinophil count, and total nasal symptom score.

The results of these studies are partially in conflict with Amin et al,53 who found no correlation between IL-17 and the patients symptom scores, although AR patients have significant higher serum levels of IL-17 than controls.

In our study, we did not report a correlation between IL-17 and total IgE. Huang et al,45 documented that IL-17 level was positively related to the level of total IgE, and the serum level of IL-17 and IL-23 in the AR patients were markedly higher than those in healthy subjects.

We are aware that one of the limitations of the current study is the small sample size of the study population, and large-scale multicenter studies should be performed to further elucidate the importance of measuring serum lipid profile in AR patients, and including pediatrics where AR is more prevalent. The disease duration of AR was not reported in the current study. In addition, longitudinal studies might aid in a better understanding of the causal relationship between dyslipidemia and AR, to determine whether AR is preceded by dyslipidemia or the other way round. The role of cytokines as IL-17A as a biomarker of AR severity and its role in dyslipidemia should be further elucidated. Furthermore, early detection of dyslipidemia in AR patients may help in the prevention of long-term future cardiovascular morbidity and mortality in AR patients.

Measuring of serum lipid profile and IL-17A in AR patients could be a potential indicator of severe disease, and future research ought to explore the impact of timely treatment of dyslipidemia on severity of AR and QoL of patients.

The research ethics committee of Zagazig University approved the study (IRB number 6222-25-6-2020), and an informed verbal consent was obtained from all participants.

We thank all patients who participated in the study.

All authors made substantial contributions to conception and design, acquisition of data, or analysis and interpretation of data; took part in drafting the article or revising it critically for important intellectual content; agreed to submit to the current journal; gave final approval of the version to be published; and agree to be accountable for all aspects of the work.

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

The authors report no conflicts of interest in this work.

1. Seidman MD, Gurgel RK, Lin SY, et al. Clinical practice guideline. Otolaryngol Neck Surg. 2015;152(2):197206. doi:10.1177/0194599814562166

2. Meltzer EO. Allergic rhinitis: burden of illness, quality of life, comorbidities and control. Immunol Allergy Clin North Am. 2016;36(2):235248. doi:10.1016/j.iac.2015.12.002

3. Cingi C, Gevaert P, Msges R, et al. Multi-morbidities of allergic rhinitis in adults: European Academy of Allergy and Clinical Immunology Task Force Report. Clin Transl Allergy. 2017;7:17. doi:10.1186/s13601-017-0153-z

4. Lin CF, Chang YH, Chien SC, Lin YH, Yeh HY. Epidemiology of dyslipidemia in the Asia Pacific Region. Int J Gerontol. 2018;12(1):26. doi:10.1016/j.ijge.2018.02.010

5. Nus M, Mallat Z. Immune-mediated mechanisms of atherosclerosis and implications for the clinic. Expert Rev Clin Immunol. 2016;12(11):12171237. doi:10.1080/1744666X.2016.1195686

6. Yang WQ. Study of the relationship between IL-10 polymorphism and serum lipoprotein levels in Han Chinese individuals. Genet Mol Res. 2016;15(2). doi:10.4238/gmr.15028016

7. Hu X, Wang Y, Hao LY, et al. Sterol metabolism controls TH17 differentiation by generating endogenous ROR agonists. Nat Chem Biol. 2015;11(2):141147. doi:10.1038/nchembio.1714

8. Poddighe D, Brambilla I, Licari A, Marseglia GL. Pediatric rhinosinusitis and asthma. Respir Med. 2018;141:9499. doi:10.1016/j.rmed.2018.06.016

9. Monin L, Gaffen SL. Interleukin 17 family cytokines: signaling mechanisms, biological activities, and therapeutic implications. Cold Spring Harb Perspect Biol. 2018;10(4):a028522. doi:10.1101/cshperspect.a028522

10. Chiricozzi A, Guttman-Yassky E, Surez-Farias M, et al. Integrative responses to IL-17 and TNF- in human keratinocytes account for key inflammatory pathogenic circuits in psoriasis. J Invest Dermatol. 2011;131(3):677687. doi:10.1038/jid.2010.340

11. Martin DA, Towne JE, Kricorian G, et al. The emerging role of IL-17 in the pathogenesis of psoriasis: preclinical and clinical findings. J Invest Dermatol. 2013;133(1):1726. doi:10.1038/jid.2012.194

12. Murdaca G, Colombo BM, Puppo F. The role of Th17 lymphocytes in the autoimmune and chronic inflammatory diseases. Intern Emerg Med. 2011;6(6):487495. doi:10.1007/s11739-011-0517-7

13. Manti S, Cuppari C, Marseglia L, et al. Association between allergies and hypercholesterolemia: a systematic review. Int Arch Allergy Immunol. 2017;174:6776. doi:10.1159/000480081

14. Fessler MB, Jaramillo R, Crockett PW, Zeldin DC. Relationship of serum cholesterol levels to atopy in the US population. Allergy. 2010;65(7):859864. doi:10.1111/j.1398-9995.2009.02287.x

15. Ouyang F, Kumar R, Pongracic J, et al. Adiposity, serum lipid levels, and allergic sensitization in Chinese men and women. J Allergy Clin Immunol. 2009;123:9408.e10. doi:10.1016/j.jaci.2008.11.032

16. Kusunoki T, Morimoto T, Sakuma M, et al. Total and low-density lipoprotein cholesterol levels are associated with atopy in schoolchildren. J Pediatr. 2011;158:334336. doi:10.1016/j.jpeds.2010.10.009

17. Peng J, Huang Y. Meta-analysis of the association between asthma and serum levels of high-density lipoprotein cholesterol and low-density lipoprotein cholesterol. Ann Allergy Asthma Immunol. 2017;118(1):6165. doi:10.1016/j.anai.2016.09.447

18. Vinding RK, Stokholm J, Chawes BLK, Bisgaard H. Blood lipid levels associate with childhood asthma, airway obstruction, bronchial hyperresponsiveness, and aeroallergen sensitization. J Allergy Clin Immunol. 2016;137(1):6874.e4. doi:10.1016/j.jaci.2015.05.033

19. Klimek L, Bachert C, Pfaar O, et al. ARIA guideline 2019: treatment of allergic rhinitis in the German health system. Allergol Select. 2019;3(1):2250. doi:10.5414/ALX02120E

20. Bernstein IL, Li JT, Bernstein DI, et al. Allergy diagnostic testing: an updated practice parameter. Ann Allergy Asthma Immunol. 2008;100(3):S1148.

21. Li JT, Lockey RF, Bernstein IL, Portnoy JM, Nicklas RA; American Academy of Allergy Asthma and Immunology. American College of Allergy, Asthma and Immunology. Joint task force on practice parameters, allergen immunotherapy: a practice parameter. Ann Allergy Asthma Immunol. 2003;90:140. doi:10.1016/S1081-1206(10)63600-9

22. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem. 1972;18:499502. doi:10.1093/clinchem/18.6.499

23. Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults. Circulation. 2013;129(25 suppl 2):S145. doi:10.1161/01.cir.0000437738.63853.7a

24. Ference BA, Graham I, Tokgozoglu L, Catapano AL. Impact of lipids on cardiovascular health: JACC health promotion series. J Am Coll Cardiol. 2018;72(10):11411156. doi:10.1016/j.jacc.2018.06.046

25. Afshinnia F, Pennathur S. Lipids and cardiovascular risk with CKD. Clin J Am Soc Nephrol. 2020;15(1):57. doi:10.2215/CJN.13531119

26. La Mantia I, Andaloro C, Albanese PG, Varricchio A. Blood lipid levels related to allergic rhinitis: a significant association? EuroMediterranean Biomed J. 2017;12(30):144147.

27. Alwan A, Alobaidi A. Lipid profile in patients with asthma and allergic rhinitis. Int J Med Sci. 2018;1(2):924.

28. Schafer T, Ruhdorfer S, Weigl L, et al. Intake of unsaturated fatty acids and HDL cholesterol levels are associated with manifestations of atopy in adults. Clin Exp Allergy. 2003;33(10):13601367. doi:10.1046/j.1365-2222.2003.01780.x

29. Ahmed M, Madian Y, El-Tabbakh M, El-Serafi A, Nasr G, Hessam W. Correlation between dyslipidemia and severity of allergic rhinitis. Egypt J Otolaryngol. 2018;34(2):111. doi:10.4103/ejo.ejo_90_17

30. Ko SH, Jeong J, Baeg MK, et al. Lipid profiles in adolescents with and without asthma: Korea National Health and Nutrition Examination Survey data. Lipids Health Dis. 2018;17(1):158. doi:10.1186/s12944-018-0807-4

31. Yon DK, Lee SW, Ha EK, et al. Serum lipid levels are associated with allergic rhinitis, nasal symptoms, peripheral olfactory function, and nasal airway patency in children. Allergy. 2018;73(9):1905190828. doi:10.1111/all.13484

32. Craig T, McCann J, GurevichH F, Davies M. The correlation between allergic rhinitis and sleep disturbance. J Allergy Clin Immunol. 2004;114:S13945. doi:10.1016/j.jaci.2004.08.044

33. Robertson AKL, Zhou X, Strandvik B, Hansson GK. Severe hypercholesterolaemia leads to strong Th2 responses to an exogenous antigen. Scand J Immunol. 2004;59(3):285293. doi:10.1111/j.0300-9475.2004.01403.x

34. Huang SL, Lin KC, Pan WH. Dietary factors associated with physician-diagnosed asthma and allergic rhinitis in teenagers: analyses of the first Nutrition and Health Survey in Taiwan. Clin Exp Allergy. 2001;31:259264. doi:10.1046/j.1365-2222.2001.00938.x

35. Lumia M, Luukkainen P, Kaila M, et al. Maternal dietary fat and fatty acid intake during lactation and the risk of asthma in the offspring. Acta Paediatr. 2012;101:e33743. doi:10.1111/j.1651-2227.2012.02718.x

36. Raj D, Kabra SK, Lodha R. Childhood obesity and risk of allergy or asthma. Immunol Allergy Clin North Am. 2014;34:753765. doi:10.1016/j.iac.2014.07.001

37. Ciprandi G, Fenoglio D, De Amici M, Quaglini S, Negrini S, Filaci G. Serum IL-17 levels in patients with allergic rhinitis. J Allergy Clin Immunol. 2008;122(3):650651.e2. doi:10.1016/j.jaci.2008.06.005

38. Ciprandi G, De Amici M, Murdaca G, et al. Serum interleukin-17 levels are related to clinical severity in allergic rhinitis. Allergy. 2009;64(9):13751378. doi:10.1111/j.1398-9995.2009.02010.x

39. Huang X, Chen Y, Zhang F, Yang Q, Zhang G. Peripheral Th17/Treg cell-mediated immunity imbalance in allergic rhinitis patients. Braz J Otorhinolaryngol. 2014;80(2):152155. doi:10.5935/1808-8694.20140031

40. Tang J, Xiao P, Luo X, et al. Increased IL-22 level in allergic rhinitis significantly correlates with clinical severity. Am J Rhinol Allergy. 2014;28(6):e197201. doi:10.2500/ajra.2014.28.4088

41. Tsvetkova-Vicheva VM, Gecheva SP, Komsa-Penkova R, Velkova AS, Lukanov TH. IL-17 producing T cells correlate with polysensitization but not with bronchial hyperresponsiveness in patients with allergic rhinitis. Clin Transl Allergy. 2014;4(1):3. doi:10.1186/2045-7022-4-3

42. Xuekun H, Qintai Y, Yulian C, Zhang G. Correlation of gammadelta-T-cells, Th17 cells and IL-17 in peripheral blood of patients with allergic rhinitis. Asian Pac J Allergy Immunol. 2014;32(3).

43. Bayrak Degirmenci P, Aksun S, Altin Z, et al. Allergic rhinitis and its relationship with IL-10, IL-17, TGF-, IFN-, IL 22, and IL-35. Dis Markers. 2018;2018:9131432. doi:10.1155/2018/9131432

44. Ba L, Du J, Liu Y, Shang T, Yang F, Bian P. The expression and significance of interleukin-17 and the infiltrating eosinophils in nasal polyps and nasal mucous of allergic rhinitis. L J. 2010.

45. Huang X, Yang Q, Chen Y, Li P, Zhang G, Li Y. Expressions of IL-17, IL-21 and IL-23 in the serum of allergic rhinitis patients. J Med Biochem. 2011;30(4):323327. doi:10.2478/v10011-011-0025-3

46. Miossec P, Korn T, Kuchroo VK. Interleukin-17 and Type 17 Helper T cells. N Engl J Med. 2009;361(9):888898. doi:10.1056/NEJMra0707449

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Immunology

IncellDx Files Patent for COVID Long Hauler Index and Active COVID-19 Severity Score – BioSpace

Company launches http://www.covidlonghaulers.com website to facilitate immune profiling and therapy

SAN CARLOS, Calif., Feb. 3, 2021 /PRNewswire/ -- IncellDx, a leading precision medicine diagnostics company, has filed patents for algorithms identifying immunologic profiles unique to COVID long haulers and patients with severe COVID.

IncellDx has developed and patented two distinct algorithms using machine learning, built on a tailored panel of cytokines and chemokines specific for abnormalities in cytokine storm conditions and in chronic COVID patients (often referred to as COVID "long haulers"). These have been submitted for publication (pre-print available through BioRx https://www.biorxiv.org/content/10.1101/2020.12.16.423122v1).

The first algorithm generates a severity score based on analysis of hundreds of COVID-19 patients spanning the spectrum of disease severity from mild to critical. The second algorithm derived from the same cytokine/chemokine immune panel, demonstrates that the immunology of long haulers is distinct from active COVID-19. This objective algorithm offers the opportunity for precision medicine to be used by physicians as a guide in the care of COVID-19 patients.

Bruce Patterson, M.D., CEO of IncellDx, commented that "Since the beginning of the COVID-19 pandemic, IncellDx has led the way in using biomarkers to develop precision medicine approaches to therapy including the post-COVID-19 long haulers. A recent preprint of a meta-analysis suggests as many as 80% of individuals infected by COVID-19 may have at least one symptom long after infection."

IncellDx, in collaboration with Drs. Ram Yogendra and Purvi Parikh, launched the website http://www.covidlonghaulers.com on January 29, 2021. The site will serve as a resource for patients and clinicians who are dealing with the long-term complications of COVID-19. The new COVID long hauler index and severity score will likely play an important role in providing clinicians with immunological information that will aid them in caring for these patients.

Ram Yogendra, M.D. of the ECA Wellness Center, said that "through our research on chronic COVID, we recognize that there is a significant group of patients who have debilitating symptoms and complications weeks and months after the initial infection. We believe our long hauler index and treatment center are key steps in addressing this growing public health crisis."

Purvi Parikh, M.D., Immunologist, Allergist and COVID -19 researcher, stated that "as with everything in this pandemic, many of the devastating and long-term side effects of this virus are mysterious and uncertain. So much attention is paid to the death rate, but we are missing those whose quality of life has been completely changed by this terrible virus. I am happy we are at the start of a journey to help find answers for these COVID patients who continue to struggle months later. "

About IncellDx

IncellDx, Inc., located in San Carlos, California, is a single-cell, molecular diagnostics company dedicated to revolutionizing healthcare, one cell at a time. By combining molecular diagnostics with high throughput cellular analysis, the company's focus is on critical life threatening diseases in the areas of COVID-19, infectious disease and oncology/immuno-oncology, i.e., cervical, head and neck, lung, bladder, breast and prostate cancers.

CONTACT: Chris Meda, 650-777-7630

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SOURCE IncellDx, Inc.

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Immunology

The Role of the Host Immune Response in COVID-19: Friend or Foe? – Technology Networks

One of the biggest mysteries of the current pandemic is why outcomes from SARS-CoV-2 infection vary so widely between different people. Researchers are searching for clues in the host immune response to the virus.Most people who are infected with SARS-CoV-2 will clear the virus with few or no symptoms, whereas others will develop a severe illness that can lead to hospitalization and death.As with any virus, its your immune system that protects you against the deleterious consequences of an infection, says Arne Akbar, professor of immunology at University College London. But theres something about the immune system that isnt quite right in combating SARS-CoV-2 that gives these very bad outcomes in some individuals.But exactly what this immune dysfunction looks like is poorly understood and is likely to differ between patients with severe disease.It appears that if the infection isnt cleared straight away, some of the disease pathologies might be caused by the immune system rushing to try and fight it, describes Deborah Dunn-Walters, professor of immunology at the University of Surrey and chair of the British Society of Immunology COVID-19 taskforce. So its important to try and understand the balance of the immune response whats good and whats not.Unraveling the complex interactions between SARS-CoV-2 and the immune system is challenging, but hugely important in shaping our response to the virus. Our knowledge of the host immune response is already helping to identify existing drugs for treating critically ill patients. It is also underpinning work to develop novel vaccines that offer our best hope of escaping the devastating impact of the current pandemic.

The next stage is the adaptive immune response, which takes longer to get up and running but generates a highly specific response against the virus. The immune system has B cells that can produce neutralizing antibodies against the virus and T cells that can recognize and kill virus-infected cells, continues Akbar. During the lag phase, as B and T cells become activated, innate immune cells can offer some protection, but theyre not as specialized in what they do.

During the early stages of the pandemic, some people expressed concern that the host immune response to SARS-CoV-2 might deviate from the normal pattern.Its been really positive to see the data accumulate, says Lucy Walker, professor of immune regulation at University College London. Its panned out pretty much as we would expect, with most people generating antibodies and nice T-cell responses.

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But like any army, it needs to be tightly controlled, says Akbar. If its not, this can lead to autoimmune conditions, like rheumatoid arthritis or type 1 diabetes, where the immune system starts to attack a persons body tissues.

Researchers are exploring what happens when the balance starts to shift the wrong way in COVID-19, leading to the immune system turning on the host.

Its rather like autoimmunity, says Walker. Most people clear the virus with few problems and switch off the immune response but some end up with a prolonged response and immune-mediated damage.

Researchers have uncovered a variety of factors that are known to increase the risk of severe COVID-19, including age and certain pre-existing health conditions which could provide clues as to what might be going wrong.

Theres a phenomenon called inflamm-aging where people have more background inflammation as they get older, says Akbar. Interestingly, some of the pre-existing health conditions that predispose to severe COVID-19 are associated with higher levels of these inflammatory mediators.

Researchers are exploring the hypothesis that background inflammation could interfere with the bodys ability to get rid of the virus quickly without inducing tissue damage.

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This immune memory should trigger a faster and bigger response if you encounter the virus again, explains Walker. That means you should clear the infection with far fewer symptoms compared to the first time and hopefully none at all.A recent study showed that healthcare workers who have previously had COVID-19 are provided with 83% protection for at least 5 months. Another study showed that immunity may last up to eight months, indicated by the presence of neutralizing antibodies, memory B cells and T cells in the bloodstream.For the vast majority of people, once youve had it you dont tend to get it again, says Akbar. A few anecdotal cases have generated a lot of attention, but its actually only a small number of people who get reinfected.

Understanding how long protection lasts will be important for informing future vaccination strategies. Some researchers predict that immunization against SARS-CoV-2 may even generate a better immune memory compared to a natural infection.

Viruses often have ways to evade the immune response, explains Walker. Thats one of the things that SARS-CoV-2 is quite good at delaying or suppressing the initial immune response very early on in an infection, whereas vaccines dont have those characteristics.

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Weve needed to draw on pre-existing knowledge about the normal immune response and the types of immune response you want to elicit with vaccines, says Walker. And weve also relied on the availability of immunological assays to measure these effects.

Every vaccine candidate must first undergo extensive pre-clinical testing to find out whether they offer protection against the infection and the disease.

You need the immunology to assess the safety and efficacy of a candidate vaccine before taking it into clinical trials, explains Dunn-Walters. You need to monitor for the presence of neutralizing antibodies and T-cell responses that are specific to the virus.Defining whats known as the correlates of protection is key, providing scientists with the ability to assess a vaccines efficacy by measuring the immune response rather than through clinical outcomes.It gives you the tools to then look at different populations without having to challenge thousands of people with the virus, says Dunn-Walters. Once a vaccine is proven to work, it may even become unethical for people to take part in randomized placebo-controlled trials.

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Every pandemic is going to be different so you cant necessarily write a complete rule book, reflects Dunn-Walters. But we can learn lessons that will help us to be better prepared to deal with future threats.

Others emphasize the importance of investing in a breadth of basic science, which has underpinned so much of what has been achieved.

We dont know where the next problem for humanity is going to come from and what were going to need to tackle it, says Walker. But having up-to-date textbooks about the basic principles will certainly put us in the best position to succeed.

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The Role of the Host Immune Response in COVID-19: Friend or Foe? - Technology Networks

Immunology

Screening, Within and Without | In the Pipeline – Science Magazine

So Im a small-molecule drug discovery person at heart, since I started out as a synthetic organic chemist. Talking about vaccines and antibodies nonstop is a bit of a strain, then, because immunology is full of stuff thats rather far removed from good ol small-molecule ligands. Actually immunology eventually wears out everyone. Even immunologists. It just keeps on going: detail on top of detail, layer upon layer of complex, interconnected, rococo feedback loops and backup systems, repurposed evolutionary holdovers, insanely subdivided cell lineages, all the rest of it.

But in the end, even a medicinal chemist starts to feel at home in some parts of it. Because one of the key events in the adaptive immune system is exactly like one of the key events in so many small-molecule drug research programs: high-throughput screening. I know that I have a lot of people reading this who have never done any such thing, so its worth some explanation. Now, in traditional med-chem and its allied fields, HTS has been a way of life for around 30 years now (before that it was low-throughput screening!) Its had a lot of refinements and extensions, but the fundamental process has not changed one bit: round up some of your biological target (an enzyme, a receptor, an interaction between two proteins, whatever youve got), and find some setup where you can get a signal when a compound does what you want to it. Do you want to set off a signal from a receptor? Keep two proteins from coming together? Gum up the works of some enzyme? Work up some assay system where when that desired event happens, you get a signal that come up out of the noise.

It could be (and often is) a flash of fluorescence at a particular wavelength. That idea has had plenty of changes rung on it maybe youre looking at two wavelengths at the same time and checking the ratio between them. Or you can set things up where its the polarization of that fluorescent light thats telling you something. Maybe youre running things in a way where the fluorescence is already going on and your desired stuff will shut it off. You can have fluorescent probe compounds; there are whole careers involved with those things. Then there are of course fluorescent proteins (like the famous Green Fluorescent Protein), and listing the ways that those are used in assays would take us the rest of the week. Theres are physical phenomena that will allow fluorescence to be set off only when two suitable species are close enough together in space, and as you can imagine, these have been turned into workhorse assays.

Luminescence can be used in similar ways. The enzyme luciferase has been exploited six ways from Sunday, with a long list of variations. Any good screening lab has a list of their compounds that have been shown to directly interfere with the enzyme (and can thus hose up your data). We love luciferase so much that we use both the firefly kind and one from a deep-sea critter called a sea pansy because they come in both green and red versions (and sometimes you use both of those at the same time, too). That same sort of only when they come close together trick can be worked with luminescence, too. No. there are all sorts of tricks you can play with funny wavelengths of colorful light, and all sorts of interesting ways you can set up assays to emit them.

But it doesnt have to be light. A classic way to do receptor assays (and others) is to have a radioactive compound already stuck to your target. You add some of your test substance and see if it kicks any of the hot stuff off, which you read off after a filtration step: the more radioactive your filtrate, the better your compound bound to the target. You can mix radioactivity and a light-driven readout, with a scintillation proximity assay: a radioligand that gives off a beta-particle lights things up only when its next to your target, and not under other conditions.

No matter how you run any of these, the idea is to get such an assay set up so that theres a high signal-to-noise, low chances for false positives and false negatives, no need for too many picky dispensing or mixing steps to get it running, and (especially) the ability to run at the smallest scale you can handle. I well recall when doing such things in assay plates with 8 wells by 12 (96 total) was considered kind of high-tech, but for a long time now any assay that cant be shrunk down to 384 wells (1624) or 1536 (3248) has been greeted with a weary sigh and a roll of the eyes. There are legions of commercial assay kits and associated dispensers, plate-handling robots, and plate-reading machines that will assist you in getting all this going.

You want this miniaturization, of course, because you want to put the HT in the HTS. A full-deck screen at a big drug company can be a few million compounds if you pull out all the stops (which we dont so often any more, to be honest), and doing that 96 wells at a time will take you a while. Especially when you consider controls and duplicates, and youd better if you dont want to seriously waste your time. No, if youre going to screen a really impressive set of compounds, youre going to need all the help you can get. The latter 1990s and early 2000s in the drug business was a period when the high-throughput screeners and the combinatorial chemists tried to outdo each other

And heres where we get back to coronaviruses, antibodies, and vaccines. Because high-throughput screening is what goes on in your bloodstream constantly, as your adaptive immune system watches for pathogens. Everyone carries around a huge variety of different antibodies, all of which fit into some basic structural templates. No one is quite sure just how many different antibodies a person has, actually, because a real count is just an overwhelming task: the usual guesses are in the tens of billions, hundreds of billions, maybe a trillion different ones, which is a hard number to grasp. Imagine a company with a million compounds in its screening deck (OK), and then try to picture a million such companies (nope, not happening). And it might be a lot more incomprehensible than that the first link in this paragraph will take you to a paper that estimates that the available diversity for circulating antibodies is on the order of 10 to the 18th, and whats yet another factor of a million between friends? Given the combinatorial possibilities, it is beyond certain that no two humans have ever had the same repertoire of antibodies, and that no two humans ever will.

These things are floating around in your blood and being displayed on the surface of your various B cells (a mere hundred thousand or so per B cell), just waiting to see if there might someday be something that they bind to. Theyre just like a compound collection in a drug company, actually, except theyre not being stored in separate vials or wells, but are rather dumped all together in your bloodstream. And the assay conditions have been long worked out by evolution, with a huge signal/noise: activation of complement or of the various types of effector cells that respond so dramatically to the presence of antibodies bound to an antigen target.

Theres actually a screening method used in drug discovery thats broadly similar to this: DNA-encoded libraries. Thats where you build up a huge set of small molecules, each of which has its own DNA bar code attached to it. You screen these all at once, too you can hold up a small plastic Eppendorf vial that has (easily) tens of millions of different compounds in it, each with its own DNA identifier. You run the assay in a way that you pan for the potent binders, washing the less potent ones out of the system. Then after you finally knock the strong binders off with stronger conditions, you amplify and sequence their DNA barcode regions and get a reading of what small-molecule structures they must have been. That makes it sound relatively straightforward, but doing this right takes a good deal of care and a lot of data analysis of the hits at the end.

But you can see how it works in a roughly similar fashion to the way native antibodies work in our own bloodstreams. You start with a large variety of compounds, all mixed together, and you try them against a given target. When one of them binds strongly, you use some sort of amplification to pick out this rare event which is present in extremely small concentration. With DNA-encoded libraries, its getting rid of all the weaker binders by washing them off, and using PCR to make far more copies of the DNA sequences you have left. In the immune system, the amplification is built into the cellular responses, which propagate strongly through the immune system and set off further responses in turn.

The immune system is a lot more impressive, of course. Its had a long time to get better, under constant whole-organism threats of illness and death and subsequent inability to reproduce. The screening collection in any single humans bloodstream is far larger than any human efforts have ever reached, so the amplification of any given binding signal has to be a lot more robust. Thats been under serious selection pressure as well, of course: if we pick the wrong compound in a screening effort we will waste time and money, but if the immune system picks the wrong antigen to go off on, it can start attacking your own bodys tissues and kill you. The amount of infrastructure thats been built up over the millennia to avoid that is pretty intimidating all by itself.

Note that we wouldnt even be able to do the DEL trick without piggybacking on all that evolutionary work, either. The ligase enzymes that allow us to build up the DNA barcodes and the PCR that lets us amplify the DNA at the end yeah, we stole all that and repurposed it, and theres no way that you could ever get things to work without them. But its just like the fluorescent proteins mentioned above molecular biology and chemical biology depend on being able to repurpose the amazing array of tools found in living cells. Weve added plenty of our own technologies as well. No living organism does anything like electrospray mass spectrometry, Frster resonance energy transfer, NMR, surface plasmon resonance or the like. But combining what weve learned of chemistry and physics with what evolution has developed, you can run some pretty fancy systems, which are getting fancier all the time.

But for sheer library size and ability to pick out hits, nothing we humans have been able to put together rivals the adaptive immune system. Perhaps thats been one minor side effect of the pandemic: people who have taken the time to learn a bit about immunology can only come away with a sense of awe when they start to see the huge panorama of whats been going on inside their bodies for every second of their lives.

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Screening, Within and Without | In the Pipeline - Science Magazine

Immunology

Efficacy of Tezepelumab in Patients with Severe, Uncontrolled Asthma w | JAA – Dove Medical Press

Claire Emson,1 Jonathan Corren,2 Kinga Saapa,3 sa Hellqvist,4 Jane R Parnes,5 Gene Colice6

1Translational Science and Experimental Medicine, Research and Early Development, Respiratory and Immunology, BioPharmaceuticals R&D, AstraZeneca, Gaithersburg, MD, USA; 2David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA, USA; 3Biometrics, Late-Stage Development, Respiratory and Immunology, BioPharmaceuticals R&D, AstraZeneca, Warsaw, Poland; 4Biometrics, Late-Stage Development, Respiratory and Immunology, AstraZeneca, Gothenburg, Sweden; 5Amgen, Thousand Oaks, CA, USA; 6Late-Stage Development Respiratory and Immunology, BioPharmaceuticals R&D, AstraZeneca, Gaithersburg, MD, USA

Correspondence: Claire EmsonAstraZeneca, One MedImmune Way, Gaithersburg, MD, 20878, USATel +13013980304Email Claire.emson@astrazeneca.com

Background: Tezepelumab is a human monoclonal antibody that blocks thymic stromal lymphopoietin, an epithelial cytokine implicated in asthma pathogenesis, from binding to its heterodimeric receptor. In the phase 2b PATHWAY study, tezepelumab significantly reduced annualized asthma exacerbation rates (AAERs) versus placebo, irrespective of baseline disease characteristics, and improved lung function and symptom control, in adults with severe, uncontrolled asthma. This post hoc analysis assessed the efficacy of tezepelumab in adults with severe, uncontrolled asthma with and without nasal polyposis (NP).Methods: In this post hoc analysis of the PATHWAY study (NCT02054130), participants (N=550) were randomized 1:1:1:1 to receive subcutaneous tezepelumab 70 mg every 4 weeks (Q4W), 210 mg Q4W or 280 mg every 2 weeks (Q2W), or placebo Q2W, for 52 weeks. The AAER over 52 weeks and the change from baseline to week 52 in blood eosinophil count, fractional exhaled nitric oxide (FeNO) levels and serum levels of interleukin (IL)-5 and IL-13 with tezepelumab 210 mg (the phase 3 dose) and placebo were analyzed in patients grouped by self-reported presence (NP+) or absence (NP) of NP at screening.Results: At baseline, NP+ patients had higher blood eosinophil counts, higher FeNO levels and higher serum IL-5 and IL-13 levels than NP patients. Tezepelumab 210 mg reduced the AAER versus placebo to a similar extent in both NP+ and NP patients (NP+, 75% [95% confidence interval (CI): 15, 93], n=23; NP, 73% [95% CI: 47, 86], n=112). Patients treated with tezepelumab 210 mg demonstrated greater reductions in blood eosinophil count and levels of FeNO, IL-5 and IL-13 than placebo-treated patients, irrespective of NP status.Discussion: Tezepelumab reduced exacerbations and reduced type 2 inflammatory biomarkers in patients with and those without NP, supporting its efficacy in a broad population of patients with severe asthma.

Keywords: asthma, biomarkers, nasal polyps, sinusitis, tezepelumab, thymic stromal lymphopoietin

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Immunology

Scientists fear COVID-19 variant is taking the edge off vaccines – Sydney Morning Herald

Based on early studies, Pfizer has said it does not expect a significant reduction in the effectiveness of its vaccine. The company says it can quickly adjust its vaccine if necessary.

However, that is based on laboratory studies, not human data. And all four vaccines use different technologies but have an identical core component a piece of the virus spike protein they try to generate an immune response to.

Nurse Novita Sirait gives a COVID-19 vaccine to a colleague at a community health centre in Medan, North Sumatra, Indonesia.Credit:AP

Pfizers vaccine was approved for use in Australia in January, and 53.8 million doses of AstraZenecas vaccine have been bought and will be distributed over coming months.

The South African variant of the virus has been picked up eight times in Australia.

It is hard to say for sure, but you would think there is the potential they would also be reduced, said Associate Professor Corey Smith, head of translational and human immunology at the QIMR Berghofer Medical Research Institute.

He said the results suggested the virus could mutate in ways that made antibodies and vaccines less effective. But I dont think thats a real surprise, he said. Viruses always mutate.

The South African variant, known as N501Y.V2, has several mutations that in lab tests appear to change the shape of the virus spike in a way that reduces the ability of some antibodies generated from infection with the original Wuhan variant of COVID-19 from binding.

That raises concerns about reinfection, and about how well COVID-19 vaccines based on the original variant will protect against the South African variant.

Professor David Tscharke, head of the department of immunology and infectious diseases at the Australian National University, said it was always likely that we will have to chase variants by changing our vaccines.

However, he said it was not clear cut that AstraZeneca and Pfizers vaccines faced the same problems as Novavax and Johnson & Johnson.

You might guess that but the extent of that is going to be varied, he said. Although they have the same antigens, they are presented in a different way.

Virus-killing T-cells also played a role in immunity, he said, and they might allow Pfizer and AstraZenecas jabs to still offer strong protection against the variant.

Early lab evidence suggested Pfizers vaccine would be less effective against the South African variant, but would still cover the virus.

But those studies were carried out using pseudoviruses viruses manipulated to look like N501Y.V2 and were done on cells in a lab. Such studies do not always translate to humans.

Science and health explained and analysed with a rigorous focus on the evidence. Examine is a weekly newsletter by science reporter Liam Mannix. Sign up to receive it every Tuesday.

Novavax and Johnson & Johnson are the first vaccine developers to report human data on the variants.

Novavaxs trial of more than 4400 patients in South Africa reported efficacy of 49.4 per cent (excluding HIV-positive patients, efficacy rose to 60 per cent). Nearly all the cases of infection among vaccinated subjects were from the South African variant.

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Johnson & Johnsons trial of 6576 people in South Africa reported efficacy of 57 per cent; 95 per cent of infections in people vaccinated were from the South African variant.

These trials were small and the results were preliminary, experts said. South Africa also presents a unique environment to test vaccines: a runaway epidemic means people may be exposed to unusually high levels of virus.

But even with all that in mind, said Associate Professor Stuart Turville, a virologist at the Kirby Institute, the data early on, looks like the edge has been taken off by the South African variant.

What were seeing in the real world is this thing has the potential to take the edge off vaccines. Which may mean we need to update the formulation.

It is anticipated that the Pfizer and AstraZeneca vaccines will have significant efficacy against the newer strains of COVID-19, a spokesman for the Therapeutic Goods Administration said.

The vaccines work by inducing what is known as a polyclonal response a collection of immunological responses to many different parts of the COVID spike protein. In the new variants, only a limited part of the spike protein is changed, and much is unchanged. So the vaccines should still work against the main, unchanged parts to the COVID-19 spike protein.

The results from the Novavax and Johnson & Johnson vaccines cannot be directly extrapolated to the other COVID-19 vaccines, such as the Pfizer BioNTech or Oxford AZ vaccine as each vaccine produces differing immune responses in vaccinated individuals.

The experts emphasised it was important to wait for real-world data from Pfizer and AstraZeneca. It may be the vaccines different designs work better against the variant.

These vaccines also stimulate T-cell immunity although it is not clear what role that plays in protection from COVID-19.

And even a vaccine with reduced effectiveness was much better than no vaccine at all.

To put this into context, were still getting significant protection, said Professor Tscharke. We could be living in a world where all these vaccines were giving numbers like that all around the world and we would still be pretty happy.

Get our Coronavirus Update newsletter for the day's crucial developments at a glance, the numbers you need to know and what our readers are saying. Sign up to The Sydney Morning Herald's newsletter here and The Age's here.

Liam is The Age and Sydney Morning Herald's science reporter

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Scientists fear COVID-19 variant is taking the edge off vaccines - Sydney Morning Herald

Embryology

Black History Month: Monumental moments at the WSU School of Medicine – The South End

Jaila Campbell, seen here as part of the Warrior Strong campaign, is a Wayne State University medical student and a graduate of the Post-Baccalaureate Program.

February is Black History Month through the United States. The Wayne State University School of Medicine has a storied history of African Americans of its own that dates back to a mere year after the medical school was founded. Joseph Ferguson, M.D., graduated from what was then Detroit Medical College, in 1869. He became the first Black man in Detroit and most likely in Michigan to earn a medical degree.

Fast forward more than 150 years, and the school hit another milestone in 2019 the 50th anniversary of the Post-Baccalaureate Program, founded in 1969 to ensure that qualified minorities continued to have the opportunity to enter medical school. It was the first of its kind in the nation. Initially launched to address the dearth of Black students entering medical schools, the free program now immerses first-generationstudents into a year-long education in biochemistry, embryology, gross anatomy, histology and physiology. Many who graduated from the program were accepted into the WSU School of Medicine, but the program also served for several years as a major pipeline for Black students into medical schools across the nation. Today, the program accepts students from a category deemed underrepresented in medicine, which includes African Americans, Hispanic/Latino, Native American and students from socio-economically disadvantaged backgrounds.

In between, the school continued to play a major role in addressing the physician workforce in America and bridging the gap in health disparities and health outcomes.

The WSU School of Medicine was founded in 1868 by four Civil War veteran physicians. At the same time, the first medical school in the county that was open to all people, Howard University Medical Department, opened in Washington, D.C., under the direction of Civil War veteran and Commissioner of the Freedmens Bureau, Gen. Oliver Howard. One year later, in 1869, the Detroit College of Medicine and Howard University graduated their first Black physicians.

Albert Henry Johnson, M.D., became the third Black graduate of the Detroit College of Medicine, in 1893. Dr. Johnson was one of the founders of Dunbar Hospital, the first Black non-profit hospital in Detroit.

In 1926, Chester Cole Ames, M.D., graduated from the Detroit College of Medicine and Surgery. He was the first Black physician to obtain an internship in Urology at a white hospital in Detroit, but he was never allowed to join staff. Dr. Ames was Detroit's first Black intern, resident and member of the Wayne University medical faculty. He cofounded three Black hospitals in Detroit, but was never granted privileges to practice his specialty in white hospitals.

Some 17 years later, Marjorie Peebles-Meyers, M.D., graduated from the Wayne University College of Medicine, the schools first Black female graduate. She was also the first Black female resident at Detroit Receiving Hospital, the first Black chief resident at Detroit Receiving Hospital, the first Black female appointed to the WSU medical faculty and the first Black female to join a private white medical practice in Detroit. After retiring, she began a second career as the first Black female medical officer at Ford Motor Co. World Headquarters. Dr. Peebles-Meyers received many awards and honors, including induction into the Michigan Womens Hall of Fame.

The same amount of time elapsed before Black physicians Thomas Flake Sr., M.D., Class of 1951; Addison Prince, M.D.; William Gibson, M.D.; and James Collins, M.D., were appointed to the staff at Harper Hospital, thereby integrating the Detroit Medical Center hospital staff.

Only five years later, Charles Whitten, M.D.,became the first Black physician to head a department in a Detroit hospital when he was selected clinical director of Pediatrics at Detroit Receiving Hospital. He was also a founder of the aforementioned Post-Baccalaureate Program.

In 1981, Alexa Canady, M.D., became the first Black neurosurgeon in the United States. Dr. Canady went on to serve as professor in the WSU Department of Neurosurgery. She was named one of the countrys most outstanding doctors by Child magazine in 2001.

Around 1988, two School of Medicine students Don Tynes, M.D. 95, and Carolyn King, M.D. 93, -- established Reach Out to Youth to introduce children 7 to 11 in underrepresented populations to the possibility of careers in science and medicine. Since then, the hands-on, workshop- and activity-focused program has been presented annually by the School of Medicines Black Medical Association, a chapter of the Student National Medical Association.

In 1995, Professor of Pediatrics and Sickle Cell Detection and Information Center Founder Charles Vincent, M.D., was appointed to the Membership Committee of the American Medical Association, making him the first Black doctor appointed to the committee in the AMAs 147-year history.

In 2017, Cheryl Gibson Fountain, M.D., F.A.C.O.G., a 1987 graduate, was named the president of the Michigan State Medical Society. The obstetrician/gynecologist served a one-year term as the societys first Black female president.

Last November, an anti-racism educational effort led by School of Medicine Class of 2024 medical student Cedric Mutebi and third-year Internal Medicine-Pediatrics resident Selena Rodriguez, M.D., aimed at stopping racial disparities through reimagined medical education won a $10,000 grant from the Association of American Medical Colleges. The grant allowed the team to develop Healing Between the Lines, a sub-curriculum targeting upstream structural inequities that drive downstream disparities.

Today, the push for more diversity, more inclusion and the elimination of health disparities continue to shape the future of the School of Medicine, from student-led efforts to longitudinal research projects dedicated to the health of Black Americans.

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Black History Month: Monumental moments at the WSU School of Medicine - The South End

Embryology

Barbara Kay: Following the science in the controversy over when you became you – National Post

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I sympathize with their mission. Not because I am ideologically pro-life (Im not). Only that I favour informed consent in all ethics-related decisions. And deplore any systemic dumbing down of such decisions gravity through pedagogical misdirection.

In an email exchange with the authors, they told me their organization is active on social media, where they have discovered that many young people believe an embryo is just a clump of cells. They have never heard, for example, of the 23 Carnegie Stages of embryology, the gold standard for accurate scientific facts in the sexual reproduction cycle of life, which in rudimentary form provide the plot line of When You Became You.

I favour informed consent in all ethics-related decisions

The book did not strike me as in any way controversial on a first, casual reading, but during a more focused re-read, the charged word human jumped out at me: It does not matter what you look like Or even if you arent born yet. You are a human being; And from the moment your life begins, you are the same human being throughout your entire life; Just like you used to be a toddler and an infant, before that, you used to be a fetus, and before that, you were an embryo; A human fetus is simply a special name that scientists call a pre-born human being from nine weeks until birth. Well, you can see why this book has ruffled some progressive feathers.

Stanton and West worked with their China-based, best-selling illustrator over a period of months, with her name on the cover throughout their collaboration. But when the author/publisher of her previous books got wind of the project, her American representatives told the authors they had to pull the illustrators name, as it was too controversial. Since they couldnt acquire the high-resolution images they needed otherwise, Stanton and West agreed. A shame because, as noted, the illustrations are magnificent.

The book launched in November. The first printing has sold out and a number of schools in the U.S. are using it. West informs me that only 34 per cent of Canadians believe life begins at conception. Hopefully, When You Became You will find its way to many Canadian homes (maybe even schools?) and help to nudge those numbers upward.

Email: kaybarb@gmail.com | Twitter: BarbaraRKay

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Barbara Kay: Following the science in the controversy over when you became you - National Post

Neuroscience

Nerd Knowledge: The neuroscience of religion – Sapulpa Times

From a cognitive and neurobiological perspective, the scientific study of the human brains interaction with religion is fascinating. There is now a new branch of neuroscience called neurotheology. This discipline attempts to explain religious experience and behavior in neuroscientific terms.

Dr. Andrew Newberg, director of the Research Marcus Institute of Integrative Health at the Thomas Jefferson University and Hospital in Villanova, PA, has written a book, Principles of Neurotheology, which provides a novel approach to scientific and theological dialogue.

According to Newberg, neurotheology applies science and the scientific method to spirituality through brain imaging studies.

His studies show that both meditating Buddhists and praying Catholic nuns have increased activity in the frontal lobes of the brain. These areas are linked with increased focus and attention, planning skills, the ability to project into the future, and the ability to construct complex arguments.

Interestingly, nuns who pray with words, rather than relying on visualization techniques used in meditation, show increased activity in the language-processing brain areas of the subparietal lobes. Both prayer and meditation correlate with decreased activity in the parietal lobes, which are responsible for processing temporal and spatial orientation.

However, other religious exercises can have the opposite effect on the same areas of the brain.

Dr. Newberg co-authored studies which show that intense Islamic prayer, which has, as its most fundamental concept, the surrendering of ones self to God, reduces the neural activity in the prefrontal cortex, the frontal lobes, as well as the activity in the parietal lobes.

It is thought that the prefrontal cortex is involved in executive control, or willful behavior, as well as decision-making. Therefore scientists postulate it is logical that a practice that focuses on abdicating control would result in reduced activity in this brain area.

Dr. Jeff Anderson, Ph.D., a neuroradiologist from the University of Utah School of Medicine in Salt Lake City, along with his research team, examined the brains of 19 young Mormons using a functional MRI scanner.

The participants were asked to what degree they were feeling the spirit. Those who reported the most intense spiritual feelings displayed increased activity in the bilateral nucleus accumbens, the frontal attentional, and ventromedial prefrontal cortical loci.

These brain areas are associated with pleasure and reward processing and are also active when we engage in sexual activities, gamble, listen to music, or drug use. The subjects also reported feelings of physical warmth and peace.

Michael Ferguson, who was a bioengineering graduate student at the time, was the author of the first study, said: When our study participants were instructed to think about a savior, about being with their families for eternity, about their heavenly rewards, their brains and bodies physically responded.

Previous studies showed that spiritual practices raise levels of serotonin and endorphins which are neurotransmitters that are associated with a sense of happiness and well-being. Endorphins work on the opiate receptors in the brain. Thus, Such neurochemical responses to religion lend credence to that dictum, Religion is the opium of the people.

Dr. Andersn stated brain imaging technologies have matured in ways that are letting us approach questions that have been around for millennia, such as What causes the feeling that someone else is present in the room, or that we are outside of our bodies?

Prof. James Giordano, from the Georgetown University Medical Center in Washington, D.C., explained that activity in the superior parietal cortex, (which is a region in the upper part of the parietal lobe) or the prefrontal cortex increases or decreases, our bodily boundaries change.

These parts of the brain control our sense of self in relation to other objects in the world, as well as our bodily integrity; hence the out of body and extended self sensations and perceptions many people who have had mystical experiences confess to.

It is noteworthy that a study of Vietnam veterans shows that those who had suffered injuries to the brains dorsolateral prefrontal cortex were more likely to report mystical experiences and religious fundamentalism.

in the 1990s, Dr. Michael Persinger, Director of the Neuroscience Department at Laurentian University in Ontario, Canada, designed what came to be known as the God Helmet. It was a

device that was designed to simulate religious experiences by stimulating an individuals tempoparietal lobes using magnetic fields.

Out of the 2,000 participants, only one percent reported feeling, 81 percent felt a presence of some sort, and the remaining subjects felt no presence.

Newberg stresses that although neurotheology wont prove the existence of a higher power, it can provide a better understanding of what it means for a person to be religious.Neurotheology can explore how religion and spirituality affect physical and mental health in terms of beliefs and practices.

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Nerd Knowledge: The neuroscience of religion - Sapulpa Times