Lymphocyte Separation Medium (LSM
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The Expression of NOD2, NLRP3 and NLRC5 and Renal Injury in Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
Wang et al. J Transl Med (2019) 17:197 https://doi.org/10.1186/s12967-019-1949-5 Journal of Translational Medicine RESEARCH Open Access The expression of NOD2, NLRP3 and NLRC5 and renal injury in anti-neutrophil cytoplasmic antibody-associated vasculitis Luo‑Yi Wang1,2,3, Xiao‑Jing Sun1,2,3, Min Chen1,2,3* and Ming‑Hui Zhao1,2,3,4 Abstract Background: Nucleotide‑binding oligomerization domain (NOD)‑like receptors (NLRs) are intracellular sensors of pathogens and molecules from damaged cells to regulate the infammatory response in the innate immune system. Emerging evidences suggested a potential role of NLRs in anti‑neutrophil cytoplasmic antibody (ANCA)‑associated vasculitis (AAV). This study aimed to investigate the expression of nucleotide‑binding oligomerization domain con‑ taining protein 2 (NOD2), NOD‑like receptor family pyrin domain containing 3 (NLRP3) and NOD‑like receptor family CARD domain containing 5 (NLRC5) in kidneys of AAV patients, and further explored their associations with clinical and pathological parameters. Methods: Thirty‑four AAV patients in active stage were recruited. Their renal specimens were processed with immu‑ nohistochemistry to assess the expression of three NLRs, and with double immunofuorescence to detect NLRs on intrinsic and infltrating cells. Analysis of gene expression was also adopted in cultured human podocytes. The associa‑ tions between expression of NLRs and clinicopathological parameters were analyzed. Results: The expression of NOD2, NLRP3 and NLRC5 was signifcantly higher in kidneys from AAV patients than those from normal controls, minimal change disease or class IV lupus nephritis. These NLRs co‑localized with podocytes and infltrating infammatory cells. -
Striking the Right Balance in Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
Striking the Right Balance in Anti-neutrophil Cytoplasmic Antibody-Associated Vasculitis This symposium took place on 4th June 2021, as part of the European Alliance of Associations for Rheumatology (EULAR) virtual congress Speakers: Benjamin Terrier,¹ Joanna Robson,² Bernhard Hellmich³ 1. University of Paris and Hôpital Cochin, France 2. University of the West of England and Bristol Royal Infirmary, UK 3. University of Tübingen, Germany Disclosure: Terrier has been an advisory board member and/or received consulting fees/ travel expenses from AstraZeneca, Chugai, Grifols, GlaxoSmithKline, Janssen, LFB, Octapharma, Roche, and Vifor Pharma. Robson has received speaker’s fees from Roche and Vifor Pharma; and research support from Vifor Pharma. Hellmich has been an investigator in clinical trials for Ab2Bio, AbbVie, AstraZeneca, Bristol- Myers Squibb, Chemocentrix, GlaxoSmithKline, InflaRx, Kiniksa, Nippon Kayaku, Novartis, Roche, and Sanofi. He has acted as a consultant, advisory board member, and/or lecturer for AbbVie, Bristol-Myers Squibb, Boehringer Ingelheim, Chugai, GlaxoSmithKline, InflaRx, Novartis, Pfizer, Roche, and Vifor Pharma. He is also a member of the Guideline Committees for European Alliance of Associations for Rheumatology (EULAR) and the German Society of Rheumatology (DGRh). Acknowledgements: Writing assistance was provided by Helen Boreham. Support: The publication of this article was funded by Vifor Pharma. The views and opinions expressed are those of the presenters. Content was reviewed by Vifor Pharma for medical accuracy. Citation: Rheumatol. 2021;8[1]:43-50. Meeting Summary Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) causes irreversible short- and long-term damage to vital organs, particularly the kidneys and lungs. Current standard of care (SOC) for AAV, of which glucocorticoids (GC) are a lynchpin, has a number of important limitations: responses to therapy are variable, some patients fail to achieve and sustain remission, and treatment related adverse events (AE) are common. -
Stress and the Immune System Tracy B
4 World Health • 47th Yeor, No. 2, Morch-Aprill994 Stress and the immune system Tracy B. Herbert any people have the effects of factors as diverse as experienced the examinations, bereavement, divorce, Mconnection between stress unemployment, mental arithmetic, and getting sick. Colds, influenza, and looking after a relative with herpes and allergies seem worse Alzheimer's di sease. In general, when we are severely stressed at these studies find that stress is work or in the home. Others are related to changes in both the never sick until they go on vacation numbers of white blood cells in (that is, after the stress is over), and circulation and the quantity of then they spend the whole time antibody in the blood. Moreover, fighting the virus. Because of stress is associated with changes in intrinsic connections like these, the functioning of immune cells. many researchers are today That is, there is a relatively large exploring whether (and how) stress decrease in both lymphocyte and illness are actually linked. One proliferation and natural killer cell specific focus of this research is to activity in individuals who have study the effects of stress on the experienced stress. There seems to immune systems; after all, if stress A lymphocyte: stress may weaken the capacity be some connection between the affects immunity, that would be one of lymphocytes to combat infection. duration of the stress and the amount way in which stress could contribute of immune change. For example, the to illness. longer the stress, the greater the The function of the immune proliferation"- by incubating these decrease in the number of specific system is to protect us from cells for several days with types of white blood cells. -
Association Between Neutrophil-Lymphocyte Ratio and Herpes Zoster Infection in 1688 Living Donor Liver Transplantation Recipients at a Large Single Center
biomedicines Article Association between Neutrophil-Lymphocyte Ratio and Herpes Zoster Infection in 1688 Living Donor Liver Transplantation Recipients at a Large Single Center Ji-Hoon Sim, Young-Jin Moon, Sung-Hoon Kim, Kyoung-Sun Kim , Ju-Seung Lee, Jun-Gol Song * and Gyu-Sam Hwang Department of Anesthesiology and Pain Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea; [email protected] (J.-H.S.); [email protected] (Y.-J.M.); [email protected] (S.-H.K.); [email protected] (K.-S.K.); [email protected] (J.-S.L.); [email protected] (G.-S.H.) * Correspondence: [email protected]; Tel.: +82-2-3010-3869 Abstract: Liver transplantation (LT) is closely associated with decreased immune function, a contrib- utor to herpes zoster (HZ). However, risk factors for HZ in living donor LT (LDLT) remain unknown. Neutrophil-lymphocyte ratio (NLR) and immune system function are reportedly correlated. This study investigated the association between NLR and HZ in 1688 patients who underwent LDLT between January 2010 and July 2020 and evaluated risk factors for HZ and postherpetic neuralgia (PHN). The predictive power of NLR was assessed through the concordance index and an integrated discrimination improvement (IDI) analysis. Of the total cohort, 138 (8.2%) had HZ. The incidence of HZ after LT was 11.2 per 1000 person-years and 0.1%, 1.3%, 2.9%, and 13.5% at 1, 3, 5, and 10 years, Citation: Sim, J.-H.; Moon, Y.-J.; Kim, respectively. In the Cox regression analysis, preoperative NLR was significantly associated with HZ S.-H.; Kim, K.-S.; Lee, J.-S.; Song, J.-G.; (adjusted hazard ratio [HR], 1.05; 95% confidence interval [CI], 1.02–1.09; p = 0.005) and PHN (HR, Hwang, G.-S. -
Induction of Protein Citrullination and Auto-Antibodies Production In
www.nature.com/scientificreports OPEN Induction of protein citrullination and auto-antibodies production in murine exposed to nickel Received: 11 November 2015 Accepted: 21 December 2017 nanomaterials Published: xx xx xxxx Bashir M. Mohamed1,7, Noreen T. Boyle2,3, Anja Schinwald4, Bruno Murer5, Ronan Ward6, Omar K. Mahfoud1, Tatsiana Rakovich1, Kieran Crosbie-Staunton1, Steven G. Gray 7, Ken Donaldson4, Yuri Volkov1,2 & Adriele Prina-Mello 1,2 Citrullination, or the post-translational deimination of polypeptide-bound arginine, is involved in several pathological processes in the body, including autoimmunity and tumorigenesis. Recent studies have shown that nanomaterials can trigger protein citrullination, which might constitute a common pathogenic link to disease development. Here we demonstrated auto-antibody production in serum of nanomaterials-treated mice. Citrullination-associated phenomena and PAD levels were found to be elevated in nanomaterials -treated cell lines as well as in the spleen, kidneys and lymph nodes of mice, suggesting a systemic response to nanomaterials injection, and validated in human pleural and pericardial malignant mesothelioma (MM) samples. The observed systemic responses in mice exposed to nanomaterials support the evidence linking exposure to environmental factors with the development of autoimmunity responses and reinforces the need for comprehensive safety screening of nanomaterials. Furthermore, these nanomaterials induce pathological processes that mimic those observed in Pleural MM, and therefore require further investigations into their carcinogenicity. Citrullination is involved in several pathological processes in the body, including autoimmunity and tumor- igenesis. Citrullinated proteins are generated by a post-translational deimination or demethylimination of polypeptide-bound arginine by a family of Ca2+-dependent enzyme peptidylarginine deiminase (PAD)1. -
Heritability of Autoantibody Levels in a Twin Population
Virginia Commonwealth University VCU Scholars Compass Theses and Dissertations Graduate School 2009 Heritability of Autoantibody Levels in a Twin Population Amal Rastogi Virginia Commonwealth University Follow this and additional works at: https://scholarscompass.vcu.edu/etd Part of the Periodontics and Periodontology Commons © The Author Downloaded from https://scholarscompass.vcu.edu/etd/1854 This Thesis is brought to you for free and open access by the Graduate School at VCU Scholars Compass. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of VCU Scholars Compass. For more information, please contact [email protected]. School of Dentistry Virginia Commonwealth University This is to certify that the thesis prepared by Amal Rastogi, DMD, PhD entitled HERITABILITY OF AUTOANTIBODY LEVELS IN A TWIN POPULATION has been approved by his committee as satisfactory completion of the thesis requirement for the degree of Master of Science in Dentistry. John Gunsolley, DDS, MS, Professor, Department of Periodontics, VCU, School of Dentistry Harvey Schenkein, DDS, PhD, Chair, Department of Periodontics, VCU, School of Dentistry Robert Sabatini, DDS, MS, Assistant Professor, Department of Periodontics, VCU, School of Dentistry Thomas Waldrop, DDS, MS, Graduate Director, Department of Periodontics, VCU, School of Dentistry Harvey Schenkein, DDS, PhD, Chair, Department of Periodontics, VCU, School of Dentistry Laurie Carter, DDS, PhD, Director of Advanced Dental Education,VCU, School of Dentistry Dr. F. Douglas Boudinot, Dean of the Graduate School, VCU June 29, 2009 © Amal Rastogi, DMD, PhD 2009 All Rights Reserved 2 HERITABILITY OF AUTOANTIBODY LEVELS IN A TWIN POPULATION A thesis submitted in partial fulfillment of the requirements for the degree of MSD at Virginia Commonwealth University. -
Lymphocyte-Activation Gene 3 (LAG-3) Immune Pathway
Lymphocyte-Activation Gene 3 (LAG-3) About LAG-3 LAG-3 Lymphocyte-activation gene 3 (LAG-3) is an immune checkpoint receptor protein found on the cell surface of effector T cells and regulatory T cells (Tregs) and functions to control T cell response, activation and growth.1 TCR T cells are a type of white blood cell that are part of the immune system. Activation of cytotoxic T cells by antigens enables them to 1 kill unhealthy or foreign cells. Inactive T cell Antigen MHC Dendritic cell (APC) LAG-3 and LAG-3 and LAG-3 and Immune Function T Cell Exhaustion Cancer • After a T cell is activated to kill its • However, in certain situations where T • Because of its critical role in regulating target cell, LAG-3 expression is cells experience prolonged exposure to an exhaustion of cytotoxic T cells and Treg increased to turn off the immune antigen, such as cancer or chronic function, LAG-3 has become a target of response, so that the T cell does not go infection, the T cells become desensitized study in the cancer field. on to attack healthy cells.2 and lose their ability to activate and multiply in the presence of the antigen.4 • In cancer, LAG-3 expressing exhausted • Inhibition of the immune response is cytotoxic T cells and Tregs expressing accomplished through activation of • The desensitized T cell will also LAG-3 gather at tumor sites.5,6 the LAG-3 pathway, which can occur progressively fail to produce cytokines via binding of LAG-3 to a type of (proteins that assist in the immune • Preclinical studies suggest that inhibiting antigen-presenting complex called response) and kill the target cells.4 LAG-3 allows T cells to regain their MHC II. -
Understanding the Immune System: How It Works
Understanding the Immune System How It Works U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES NATIONAL INSTITUTES OF HEALTH National Institute of Allergy and Infectious Diseases National Cancer Institute Understanding the Immune System How It Works U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES NATIONAL INSTITUTES OF HEALTH National Institute of Allergy and Infectious Diseases National Cancer Institute NIH Publication No. 03-5423 September 2003 www.niaid.nih.gov www.nci.nih.gov Contents 1 Introduction 2 Self and Nonself 3 The Structure of the Immune System 7 Immune Cells and Their Products 19 Mounting an Immune Response 24 Immunity: Natural and Acquired 28 Disorders of the Immune System 34 Immunology and Transplants 36 Immunity and Cancer 39 The Immune System and the Nervous System 40 Frontiers in Immunology 45 Summary 47 Glossary Introduction he immune system is a network of Tcells, tissues*, and organs that work together to defend the body against attacks by “foreign” invaders. These are primarily microbes (germs)—tiny, infection-causing Bacteria: organisms such as bacteria, viruses, streptococci parasites, and fungi. Because the human body provides an ideal environment for many microbes, they try to break in. It is the immune system’s job to keep them out or, failing that, to seek out and destroy them. Virus: When the immune system hits the wrong herpes virus target or is crippled, however, it can unleash a torrent of diseases, including allergy, arthritis, or AIDS. The immune system is amazingly complex. It can recognize and remember millions of Parasite: different enemies, and it can produce schistosome secretions and cells to match up with and wipe out each one of them. -
Antibody (ANCA)-Associated Vasculitis Avacopan Introduction
CO-1 Avacopan for the Treatment of Anti-Neutrophil Cytoplasmic Auto- antibody (ANCA)-Associated Vasculitis ChemoCentryx, Inc. Arthritis Advisory Committee May 6, 2021 CO-2 Avacopan Introduction Thomas J. Schall, Ph.D. President, Chief Executive Officer ChemoCentryx, Inc. CO-3 Avacopan: First-in-Class, Targeted Therapy for ANCA-Associated Vasculitis ANCA-associated vasculitis is rare, severe, and often fatal autoimmune disease Anti-neutrophil cytoplasmic auto-antibodies (ANCA) involved in pathogenesis Inflammation of small vessels, can affect any organ Commonly affects kidneys Glucocorticoid treatment associated with significant toxicities Despite current therapies, > 1 in 10 patients die within first year of diagnosis1,2 1. Heijl et al., 2017; 2. Little et al., 2010 CO-4 Central Role of C5a in Pathogenesis of ANCA-Associated Vasculitis Jennette and Falk, 2014 CO-5 Avacopan: Highly Potent and Selective C5aR Inhibitor Avacopan avoids long-term 1 biological consequences of ‘upstream’ complement inhibition 1 Does not block C5b-9 production; leaves host defense mechanism C5aC5a AntibodiesAntibodies 2 membrane attack complex (MAC) in place C6-C9C6-C9 AvacopanAvacopan Preserves beneficial 3 functions of C5L2 pathway C5aR Leukocyte migration and signaling Leukocyte trafficking, Cell lysis migration and (i.e., Neisseria control activation Beneficial Targets ‘downstream' anti-inflammatoryanti-inflammatory 4 effect complement pathway Adaptive Phagocytosis 4 3 2 signaling and clearance CO-6 Avacopan in ANCA-Associated Vasculitis Pirow Bekker, MD, PhD Clinical Lead Avacopan Clinical Development Program ChemoCentryx, Inc. CO-7 Avacopan Proposed Indication and Dose Proposed Indication …for the treatment of adult patients with anti-neutrophil cytoplasmic auto-antibody (ANCA)-associated vasculitis (granulomatosis with polyangiitis and microscopic polyangiitis). -
Degradation of Neutrophil Extracellular Traps Is Decreased in Patients with Antiphospholipid Syndrome J
Degradation of neutrophil extracellular traps is decreased in patients with antiphospholipid syndrome J. Leffler1, L. Stojanovich2, Y. Shoenfeld3, G. Bogdanovic2, R. Hesselstrand4, A.M. Blom1 1Dept. of Laboratory Medicine, Section of Medical Protein Chemistry, Lund University, Malmö, Sweden; 2Dept. of Internal Medicine, “Bezhanijska Kosa” University Medical Center, Belgrade, Serbia; 3Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel Aviv, Israel; 4Dept. of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden. Abstract Objective A decreased ability to degrade neutrophil extracellular traps (NETs) is seen in a subgroup of patients with systemic lupus erythematosus (SLE) and correlates with the presence of autoantibodies. Antiphospholipid syndrome (APS) can develop secondary to SLE or as a primary disease. In the current study we investigated the ability of sera from patients with APS to degrade NETs. The presence of antibodies against NETs and neutrophil remnants were also determined in the same patients. Methods In the study, 106 patients with APS (73 primary and 33 secondary), 76 patients with systemic sclerosis (SSc) and 77 healthy donors as control samples were included. NETs generated from neutrophils isolated from healthy volunteers were incubated with patient sera, followed by measurement of degraded NETs or deposited IgG. Results Sera of APS patients had a decreased ability to degrade NETs compared to healthy controls, with no difference between primary and secondary APS. Sera from SSc patients did not differ significantly from healthy controls in the ability to degrade NETs. A decreased degradation of NETs correlated weakly to increased levels of antibodies against NETs/ neutrophil remnants in patients with primary APS, but stronger in patients with secondary APS. -
Belimumab (Benlysta®)
Policy Medical Policy Manual Approved Revision: Do Not Implement until 8/31/21 Belimumab (Benlysta®) NDC CODE(S) 49401-0101-XX BENLYSTA 120MG Solution Reconstituted (GLAXO SMITH KLINE) 49401-0102-XX BENLYSTA 400MG Solution Reconstituted (GLAXO SMITH KLINE) DESCRIPTION Belimumab is a human IgG1 monoclonal antibody specific for soluble human B lymphocyte stimulator protein (BLyS), a B cell survival factor. It is produced by recombinant DNA technology in a mammalian cell expression system. Belimumab does not bind to B cells directly but blocks access of soluble BLyS to its receptors on B cells. This inhibits the survival of B cells and reduces the differentiation of B cells into immunoglobulin-producing plasma cells. Treatment with belimumab leads to reductions in circulating CD19+, CD20+, naïve and activated B cells along with plasmacytoid cells and the systemic lupus erythematosus (SLE) B-cell subset. POLICY Belimumab for the treatment of the following is considered medically necessary if the medical appropriateness criteria are met. (See Medical Appropriateness below.) o Systemic Lupus Erythematosus (SLE) o Lupus Nephritis Belimumab or the treatment of other conditions/diseases, including, but not limited to, Active Central Nervous System Lupus is considered investigational. MEDICAL APPROPRIATENESS INITIAL APPROVAL CRITERIA Patient is at least 18 years of age (unless otherwise specified); AND Universal Criteria Patient must not have an active infection; AND Patient has not received a live vaccine within 30 days before starting or -
Early Lymphocyte Recovery Predicts Longer Survival After Autologous Peripheral Blood Stem Cell Transplantation in Multiple Myeloma
Bone Marrow Transplantation (2006) 37, 1037–1042 & 2006 Nature Publishing Group All rights reserved 0268-3369/06 $30.00 www.nature.com/bmt ORIGINAL ARTICLE Early lymphocyte recovery predicts longer survival after autologous peripheral blood stem cell transplantation in multiple myeloma H Kim1, H-J Sohn2, S Kim2, J-S Lee2, W-K Kim2 and C Suh2 1Division of Hematology-Oncology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea and 2Division of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea To understand the prognostic value of lymphocyte Although the use of allogeneic hematopoietic stem cell recovery after autologous peripheral blood stem cell transplantation has been increasing, autologous stem cell transplantation (APBSCT), we performed a retrospective transplantation (ASCT) remains the standard therapeutic study of 59 newly diagnosed multiple myeloma (MM) modality for MM.1–3 The main drawback of ASCT is its patients who underwent frontline APBSCT. Conditioning high relapse rate. Because immune-mediated tumor eradi- regimens were melphalan 100 mg/m2 for 2 days. Follow- cation may lower the relapse rate associated with ASCT, ing APBSCT, all patients showed complete or partial there is increasing interest in immune reconstitution response. Median follow-up time was 29.57 months and following ASCT.4–9 In support of this, a relationship median recovery of absolute lymphocyte count (ALC) between lymphocyte recovery after ASCT and relapse rate X1000/mm3 was 23 days. Univariate analysis revealed or survival has been observed in many diseases, suggesting that significant predictors of overall survival (OS) that early lymphocyte recovery associated with immune included bone marrow (BM) plasma cells p40% at reconstitution can act against residual disease progres- diagnosis (P ¼ 0.0243) and recovery of ALC X1000/mm3 sion.10–17 by day þ 23 (P ¼ 0.0156).