Difference Between Hypersensitivity and Autoimmunity Key Difference – Hypersensitivity Vs Autoimmunity
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Primary Sjogren Syndrome: Focus on Innate Immune Cells and Inflammation
Review Primary Sjogren Syndrome: Focus on Innate Immune Cells and Inflammation Chiara Rizzo 1, Giulia Grasso 1, Giulia Maria Destro Castaniti 1, Francesco Ciccia 2 and Giuliana Guggino 1,* 1 Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties, Rheumatology Section, University of Palermo, Piazza delle Cliniche 2, 90110 Palermo, Italy; [email protected] (C.R.); [email protected] (G.G.); [email protected] (G.M.D.C.) 2 Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, Via L. De Crecchio 7, 80138 Naples, Italy; [email protected] * Correspondence: [email protected]; Tel.: +39-091-6552260 Received: 30 April 2020; Accepted: 29 May 2020; Published: 3 June 2020 Abstract: Primary Sjogren Syndrome (pSS) is a complex, multifactorial rheumatic disease that mainly targets salivary and lacrimal glands, inducing epithelitis. The cause behind the autoimmunity outbreak in pSS is still elusive; however, it seems related to an aberrant reaction to exogenous triggers such as viruses, combined with individual genetic pre-disposition. For a long time, autoantibodies were considered as the hallmarks of this disease; however, more recently the complex interplay between innate and adaptive immunity as well as the consequent inflammatory process have emerged as the main mechanisms of pSS pathogenesis. The present review will focus on innate cells and on the principal mechanisms of inflammation connected. In the first part, an overview of innate cells involved in pSS pathogenesis is provided, stressing in particular the role of Innate Lymphoid Cells (ILCs). Subsequently we have highlighted the main inflammatory pathways, including intra- and extra-cellular players. -
Autoimmunity and Organ Damage in Systemic Lupus Erythematosus
REVIEW ARTICLE https://doi.org/10.1038/s41590-020-0677-6 Autoimmunity and organ damage in systemic lupus erythematosus George C. Tsokos ✉ Impressive progress has been made over the last several years toward understanding how almost every aspect of the immune sys- tem contributes to the expression of systemic autoimmunity. In parallel, studies have shed light on the mechanisms that contribute to organ inflammation and damage. New approaches that address the complicated interaction between genetic variants, epigen- etic processes, sex and the environment promise to enlighten the multitude of pathways that lead to what is clinically defined as systemic lupus erythematosus. It is expected that each patient owns a unique ‘interactome’, which will dictate specific treatment. t took almost 100 years to realize that lupus erythematosus, strongly to the heterogeneity of the disease. Several genes linked to which was initially thought to be a skin entity, is a systemic the immune response are regulated through long-distance chroma- Idisease that spares no organ and that an aberrant autoimmune tin interactions10,11. Studies addressing long-distance interactions response is involved in its pathogenesis. The involvement of vital between gene variants in SLE are still missing, but, with the advent organs and tissues such as the brain, blood and the kidney in most of new technologies, such studies will emerge. patients, the vast majority of whom are women of childbearing age, Better understanding of the epigenome is needed to under- impels efforts to develop diagnostic tools and effective therapeu- stand how it supplements the genetic contribution to the dis- tics. The prevalence ranges from 20 to 150 cases per 100,000 peo- ease. -
Pathophysiology of Immune Thrombocytopenic Purpura: a Bird's-Eye View
Egypt J Pediatr Allergy Immunol 2014;12(2):49-61. Review article Pathophysiology of immune thrombocytopenic purpura: a bird's-eye view. Amira Abdel Moneam Adly Pediatrics Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt ABSTRACT and B lymphocytes (including T-helper, T- Immune thrombocytopenic purpura (ITP) is a cytotoxic, and T-regulatory lymphocytes) 6. common autoimmune disorder resulting in isolated The triggering event for ITP is unknown7, but thrombocytopenia. It is a bleeding disorder continued research is providing new insights into characterized by low platelet counts due to decreased the underlying immunopathogenic processes as well platelet production as well as increased platelet as the cellular and molecular mechanisms involved destruction by autoimmune mechanisms. ITP can in megakaryocytopoiesis and platelet turnover. present either alone (primary) or in the setting of other Although historically ITP-associated thrombo- conditions (secondary) such as infections or altered cytopenia was attributed solely to increased rates of immune states. ITP is associated with a loss of destruction of antibody- coated platelets, it has tolerance to platelet antigens and a phenotype of become evident that suboptimal platelet production accelerated platelet destruction and impaired platelet also plays a role 8. production. Although the etiology of ITP remains Bleeding is due to decreased platelet production unknown, complex dysregulation of the immune as well as accelerated platelet destruction mediated system is observed in ITP patients. Antiplatelet in part by autoantibody-based destruction antibodies mediate accelerated clearance from the mechanisms9. Most autoantibodies in ITP are circulation in large part via the reticuloendothelial isotype switched and harbor somatic mutations10, (monocytic phagocytic) system. -
B Cell Activation and Escape of Tolerance Checkpoints: Recent Insights from Studying Autoreactive B Cells
cells Review B Cell Activation and Escape of Tolerance Checkpoints: Recent Insights from Studying Autoreactive B Cells Carlo G. Bonasia 1 , Wayel H. Abdulahad 1,2 , Abraham Rutgers 1, Peter Heeringa 2 and Nicolaas A. Bos 1,* 1 Department of Rheumatology and Clinical Immunology, University Medical Center Groningen, University of Groningen, 9713 Groningen, GZ, The Netherlands; [email protected] (C.G.B.); [email protected] (W.H.A.); [email protected] (A.R.) 2 Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, 9713 Groningen, GZ, The Netherlands; [email protected] * Correspondence: [email protected] Abstract: Autoreactive B cells are key drivers of pathogenic processes in autoimmune diseases by the production of autoantibodies, secretion of cytokines, and presentation of autoantigens to T cells. However, the mechanisms that underlie the development of autoreactive B cells are not well understood. Here, we review recent studies leveraging novel techniques to identify and characterize (auto)antigen-specific B cells. The insights gained from such studies pertaining to the mechanisms involved in the escape of tolerance checkpoints and the activation of autoreactive B cells are discussed. Citation: Bonasia, C.G.; Abdulahad, W.H.; Rutgers, A.; Heeringa, P.; Bos, In addition, we briefly highlight potential therapeutic strategies to target and eliminate autoreactive N.A. B Cell Activation and Escape of B cells in autoimmune diseases. Tolerance Checkpoints: Recent Insights from Studying Autoreactive Keywords: autoimmune diseases; B cells; autoreactive B cells; tolerance B Cells. Cells 2021, 10, 1190. https:// doi.org/10.3390/cells10051190 Academic Editor: Juan Pablo de 1. -
Mechanisms Governing Anaphylaxis: Inflammatory Cells, Mediators
International Journal of Molecular Sciences Review Mechanisms Governing Anaphylaxis: Inflammatory Cells, Mediators, Endothelial Gap Junctions and Beyond Samantha Minh Thy Nguyen 1, Chase Preston Rupprecht 2, Aaisha Haque 3, Debendra Pattanaik 4, Joseph Yusin 5 and Guha Krishnaswamy 1,3,* 1 Department of Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27106, USA; [email protected] 2 The Rowan School of Osteopathic Medicine, Stratford, NJ 08084, USA; [email protected] 3 The Bill Hefner VA Medical Center, Salisbury, NC 27106, USA; [email protected] 4 Division of Allergy and Immunology, UT Memphis College of Medicine, Memphis, TN 38103, USA; [email protected] 5 The Division of Allergy and Immunology, Greater Los Angeles VA Medical Center, Los Angeles, CA 90011, USA; [email protected] * Correspondence: [email protected] Abstract: Anaphylaxis is a severe, acute, life-threatening multisystem allergic reaction resulting from the release of a plethora of mediators from mast cells culminating in serious respiratory, cardiovascular and mucocutaneous manifestations that can be fatal. Medications, foods, latex, exercise, hormones (progesterone), and clonal mast cell disorders may be responsible. More recently, novel syndromes such as delayed reactions to red meat and hereditary alpha tryptasemia have been described. Anaphylaxis manifests as sudden onset urticaria, pruritus, flushing, erythema, Citation: Nguyen, S.M.T.; Rupprecht, angioedema (lips, tongue, airways, periphery), myocardial dysfunction (hypovolemia, distributive -
B Cell Checkpoints in Autoimmune Rheumatic Diseases
REVIEWS B cell checkpoints in autoimmune rheumatic diseases Samuel J. S. Rubin1,2,3, Michelle S. Bloom1,2,3 and William H. Robinson1,2,3* Abstract | B cells have important functions in the pathogenesis of autoimmune diseases, including autoimmune rheumatic diseases. In addition to producing autoantibodies, B cells contribute to autoimmunity by serving as professional antigen- presenting cells (APCs), producing cytokines, and through additional mechanisms. B cell activation and effector functions are regulated by immune checkpoints, including both activating and inhibitory checkpoint receptors that contribute to the regulation of B cell tolerance, activation, antigen presentation, T cell help, class switching, antibody production and cytokine production. The various activating checkpoint receptors include B cell activating receptors that engage with cognate receptors on T cells or other cells, as well as Toll-like receptors that can provide dual stimulation to B cells via co- engagement with the B cell receptor. Furthermore, various inhibitory checkpoint receptors, including B cell inhibitory receptors, have important functions in regulating B cell development, activation and effector functions. Therapeutically targeting B cell checkpoints represents a promising strategy for the treatment of a variety of autoimmune rheumatic diseases. Antibody- dependent B cells are multifunctional lymphocytes that contribute that serve as precursors to and thereby give rise to acti- cell- mediated cytotoxicity to the pathogenesis of autoimmune diseases -
Ii Vasclitides
ا يمون وپات وژنز واسکوليتھااکلتا Vascliiitides: The Immunopa tho genes is دکتر محمدمھدی محمدی LMD, PhD, MPH ([email protected]) The 7th International 12th National Congress on Quality Improvement in Clinical Laboratories 28 Farvardin 1393 / 17April 2014 , Tehran, Iran A small spoonful of Terminology (in Farsi بيماريزايی) – .path·o·gen·e·sis, n • – the ppp(roduction and development of disease (events and reactions and other pathologic mechanisms) . Also, pa·thog·e·ny !?! (in Farsi بيماريزايی) _ .path·o·ge·nic·i·ty, n • – the disease-producing capacity of a pathogen. [PATHOGENIC + -ITY] • vir·u·lence, n. – the relative ability of a microorganism to cause disease; degree of pathogenicity. • Vasculitis, n. (vasculitides, plural) – a general term for vessel wall inflammation, systemic or localized, immune-mediated or directly invaded by microbes. • Infections may indirectly generate vasculitis, e.g. through IC formation or by X_reaction. Note that immunosuppressive therapy is only appropriate for --?– type! • WHAT R the IMMUNE MECHANISMS in VASCULITIS? افراط تعادل تفريط Immunodeficiency Allergy (& Infection) Defence Immunodeficiency Surveillance Autoimmunity (& Malignancy) Homostasis ?! Some Inter-related Concepts Immunological Vasculitis Hypersensitivity Auoimmunity Tolerance EDUCATION? Tolerance in different classic Txtbks of Immunology (Abbas, Benjamini, Janeway, Kuby, Roitt, Stites …) • Tolerance (by C&M Immunology): – Unresponsiveness of the adaptive immune system to antigens, as a result of inactivation or death of antigen-specific lymphocytes, induced by exposure to the antigens. – (()Active) Unresponsiveness of the (()HEALTHY) adappytive immune system to (selected) antigens, as a result of (i.e. MECHANISMS:) inactivation or death of antigen-specific lymphocytes, induced by exposure to those antigens. • Tolerance to self antigens is a normal feature of the adaptive immune system, but tolerance to foreign antigens may be induced undtiditiftider certain conditions of antigen exposure. -
2 Allergy, Immunodeficiency, Autoimmunity and COVID-19
2 Allergy, Immunodeficiency, Autoimmunity and COVID-19 Vaccination Frequently Asked Questions (FAQ) 17 February 2021 This information has been developed by ASCIA, the peak professional body of clinical immunology/allergy specialists in Australia and New Zealand, to answer questions regarding COVID-19 vaccination in relation to allergy, immunodeficiency and autoimmunity. ASCIA will update this FAQ when new information is available. 1. Why is the COVID-19 vaccination program important? Vaccination is an important way to reduce the risk of developing infectious diseases which can easily spread. This includes COVID-19, which is caused by infection with the SARS-CoV-2 coronavirus. Immunity occurs after the vaccine stimulates a person’s immune system to make antibodies (immunoglobulins) to help protect the body from future infections. This means that if a person is vaccinated, they will be less likely to get COVID-19. Even if a person does get infected, it is likely to be a milder illness. Public health measures and restrictions that were implemented by the Australian and New Zealand governments since March 2020 have been successful in controlling the spread of COVID-19 in our countries. However, the COVID-19 pandemic has been a major cause of illness and deaths in other countries. This means that vaccination programs are required throughout the world, including Australia and New Zealand. 2. Which COVID-19 vaccines have been approved in Australia and New Zealand? Pfizer/BioNTech COMIRNATY mRNA-based COVID-19 vaccine has been provisionally approved by the Therapeutic Goods Administration (TGA), part of the Australian Government Department of Health, and by Medsafe in New Zealand for people 16 years and older. -
Food Fact Sheet: Food Allergy and Food Intolerance
Food Fact Sheet: Food Allergy and Food Intolerance Having to avoid certain foods in your diet can be difficult. But there are a few simple things you can do to help you manage your food allergies - allowing you to stay safe, continue to participate in fun activities and enjoy your food. What is the difference between food allergy and food intolerance? For some people, eating certain foods can lead to an unpleasant and sometimes dangerous physical reaction. The term used to describe all types of reactions to foods is ‘food hypersensitivity’. A 'food allergy' is a reaction involving the immune system (the body’s defence against foreign bodies). Those that do not involve the immune system are often called a ‘food intolerance’. It is important to identify and manage foods that trigger any symptoms in an appropriate way. Food allergy Proteins within foods can trigger immediate (within two hours) or delayed symptoms (up to several days later). Immediate food allergy (IgE mediated food allergy) Immediate reactions to foods occur when your immune system reacts to a normally harmless protein in food, due to the creation of Immunoglobulin E (IgE). This results in the release of chemicals (e.g. histamine) which trigger allergic symptoms. These symptoms are usually in the skin (itching/swelling), or gut (vomiting, diarrhoea). Other symptoms can include breathing problems and in rare cases an extreme allergic reaction called anaphylaxis. Delayed food allergy (non IgE mediated food allergy) Delayed reactions to foods still involve your immune system, but there is a different type of immune reaction involved. Symptoms typically occur in the gut (vomiting, diarrhoea, constipation) and/or the skin (atopic eczema). -
Allergy, Hypersensitivity, Angioedema, and Anaphylaxis Episode Overview
CrackCast Show Notes –Allergy and Anaphylaxis – October 2017 www.canadiem.org/crackcast Chapter 109 – Allergy, Hypersensitivity, Angioedema, and Anaphylaxis Episode Overview Key Points: 1. A history of sudden urticarial rash accompanied by respiratory difficulty, abdominal pain, or hypotension, strongly favors the diagnosis of anaphylaxis. 2. Epinephrine is the first-line treatment in patients with anaphylaxis: give it immediately. 3. There are no absolute contraindications to the use of epinephrine in the setting of anaphylaxis. 4. Antihistamines and corticosteroids are second- and third-line agents in the management of anaphylaxis and should not replace or precede epinephrine. 5. Consider prolonged observation or admission for patients who: a. Experience protracted anaphylaxis, hypotension, or airway involvement; b. Receive IV epinephrine or more than two doses of IM epinephrine; c. Or have poor outpatient social support. 6. Patients discharged after an anaphylactic event should be prescribed an EpiPen and instructed on its use. 7. Patients with refractory hypotension may require glucagon (receiving beta-blockage) or a continuous IV epinephrine infusion. 8. Non-histaminergic angioedema (non-allergic angioedema) does not typically respond to epinephrine and antihistamines. New drugs, including berinert, icatibant, ecallantide, and Ruconest have been approved for use in HAE. FFP has been used with varying success in HAE, ACID, and ACE inhibitor–induced angioedema. NOTE: ACID: acquired C1 esterase deficiency (ACED) Core Questions: 1. List the four types of Gell and Coombs classifications of immune reaction and give examples of each 2. List four etiologic agents causing anaphylaxis by immunologic mechanisms 3. List six mediators of anaphylaxis and their physiologic actions and clinical manifestations 4. -
Hypersensitivity Reactions (Types I, II, III, IV)
Hypersensitivity Reactions (Types I, II, III, IV) April 15, 2009 Inflammatory response - local, eliminates antigen without extensively damaging the host’s tissue. Hypersensitivity - immune & inflammatory responses that are harmful to the host (von Pirquet, 1906) - Type I Produce effector molecules Capable of ingesting foreign Particles Association with parasite infection Modified from Abbas, Lichtman & Pillai, Table 19-1 Type I hypersensitivity response IgE VH V L Cε1 CL Binds to mast cell Normal serum level = 0.0003 mg/ml Binds Fc region of IgE Link Intracellular signal trans. Initiation of degranulation Larche et al. Nat. Rev. Immunol 6:761-771, 2006 Abbas, Lichtman & Pillai,19-8 Factors in the development of allergic diseases • Geographical distribution • Environmental factors - climate, air pollution, socioeconomic status • Genetic risk factors • “Hygiene hypothesis” – Older siblings, day care – Exposure to certain foods, farm animals – Exposure to antibiotics during infancy • Cytokine milieu Adapted from Bach, JF. N Engl J Med 347:911, 2002. Upham & Holt. Curr Opin Allergy Clin Immunol 5:167, 2005 Also: Papadopoulos and Kalobatsou. Curr Op Allergy Clin Immunol 7:91-95, 2007 IgE-mediated diseases in humans • Systemic (anaphylactic shock) •Asthma – Classification by immunopathological phenotype can be used to determine management strategies • Hay fever (allergic rhinitis) • Allergic conjunctivitis • Skin reactions • Food allergies Diseases in Humans (I) • Systemic anaphylaxis - potentially fatal - due to food ingestion (eggs, shellfish, -
Immune Pathology Immune System Functions Reactivity to Tolerance Nonshared Ag to Self-Ag
Immune Pathology Immune system functions reactivity to tolerance nonshared Ag to self-Ag reduction pErVeRsIoN malfunction immunodeficiency hypersensitivity autoimmune diseases Hypersensitivity Hypersensitivity - excessive or inadequate manifestation adaptive immune of reactions Can manifest as local and systemic reactions Hypersensitivity Type Synonym Immunological mechanisms I IgE-mediated, anaphylactic, IgE-mediated degranulation of mast reaginic, HIS (blood cells dyscrasia) II antibody-dependent Cytotoxic antibodies activate cytotoxicity complement, which leads to cell lysis III immune complex Immune complexes activate leukocytes IV cell-mediated, delayed-type Cytokine production by hypersensitivity macrophages and lymphocytes V antibody-dependent Antibodies alter functional state of functional changes cells by interacting with its receptor Type I hypersensitivity • Speed of reaction - seconds or minutes • IgE-mediated • Chemical mediators of damage - vasoactive products of mast cells / basophils (histamine, arachidonic acid derivatives) • Mechanism - accumulation of of neutrophils, unstriated muscle spasm Type I hypersensitivity • bronchial asthma (some forms) • anaphylactic shock • Urticaria • Quincke's edema • dietary allergy • nasal allergy • allergic conjunctivitis Mast cell Аг Synthesis and secretion: leukotrienes (LTC4, LTB4), prostaglandins (PGD2), degranulation: IL-3, 4,5,6 histamine Platelet-activating factor serotonin (PAF) eotoxin Type I hypersensitivity Morphological manifestations IHS: • exudative alterative inflammation