Introduction to the Immune System and Immunology
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Urticaria Is a Skin Condition Commonly Known As Hives. It Produces an Itchy Rash That Tends to Come and Go and Can Last for a Variable Period of Time
Hives Also known as Urticaria What is urticaria? Urticaria is a skin condition commonly known as hives. It produces an itchy rash that tends to come and go and can last for a variable period of time. The condition can be acute (lasting less than 6 weeks) or chronic (lasting longer than 6 weeks). Most cases of urticaria have no known cause. What causes urticaria? Urticaria occurs when certain substances such as histamine are released from specific cells in the skin. This process is usually triggered by various immunologic mechanisms, most commonly involving the presee of irulatig IgE atiodies, although other pathays ay also e ioled. The ause of this iuologi triggerig is uko i the ajority of ases, ut a soeties e associated with various types of infections, chronic immunologic diseases or allergy to foods or medications. The use of intravenous dyes during some radiological tests can sometimes trigger urticaria as well. Physical urticaria is a type of urticaria that may be caused by exposure of the skin to cold, heat, pressure or rubbing. What does urticaria look like? Urticaria typically looks like a raised rash that may be a normal skin colour or pinkish or red in colour. The rash may occur anywhere on the body and often starts off as small round spots that quickly enlarge and spread. The rash can be very itchy but it usually only lasts for a few hours before settling, and eventually resolving completely within 24 to 48 hours. Which other problems may occur with urticaria? A viral illness can occur before urticaria develops, especially in children. -
IFM Innate Immunity Infographic
UNDERSTANDING INNATE IMMUNITY INTRODUCTION The immune system is comprised of two arms that work together to protect the body – the innate and adaptive immune systems. INNATE ADAPTIVE γδ T Cell Dendritic B Cell Cell Macrophage Antibodies Natural Killer Lymphocites Neutrophil T Cell CD4+ CD8+ T Cell T Cell TIME 6 hours 12 hours 1 week INNATE IMMUNITY ADAPTIVE IMMUNITY Innate immunity is the body’s first The adaptive, or acquired, immune line of immunological response system is activated when the innate and reacts quickly to anything that immune system is not able to fully should not be present. address a threat, but responses are slow, taking up to a week to fully respond. Pathogen evades the innate Dendritic immune system T Cell Cell Through antigen Pathogen presentation, the dendritic cell informs T cells of the pathogen, which informs Macrophage B cells B Cell B cells create antibodies against the pathogen Macrophages engulf and destroy Antibodies label invading pathogens pathogens for destruction Scientists estimate innate immunity comprises approximately: The adaptive immune system develops of the immune memory of pathogen exposures, so that 80% system B and T cells can respond quickly to eliminate repeat invaders. IMMUNE SYSTEM AND DISEASE If the immune system consistently under-responds or over-responds, serious diseases can result. CANCER INFLAMMATION Innate system is TOO ACTIVE Innate system NOT ACTIVE ENOUGH Cancers grow and spread when tumor Certain diseases trigger the innate cells evade detection by the immune immune system to unnecessarily system. The innate immune system is respond and cause excessive inflammation. responsible for detecting cancer cells and This type of chronic inflammation is signaling to the adaptive immune system associated with autoimmune and for the destruction of the cancer cells. -
Four Diseases, PLAID, APLAID, FCAS3 and CVID and One Gene
Four diseases, PLAID, APLAID, FCAS3 and CVID and one gene (PHOSPHOLIPASE C, GAMMA-2; PLCG2 ) : striking clinical phenotypic overlap and difference Necil Kutukculer1, Ezgi Yilmaz1, Afig Berdeli1, Raziye Burcu G¨uven Bilgin1, Ayca Aykut1, Asude Durmaz1, Ozgur Cogulu1, G¨uzideAksu1, and Neslihan Karaca1 1Ege University Faculty of Medicine May 15, 2020 Abstract We suggest PLAID,APLAID and FCAS3 have to be considered as same diseases,because of our long-term clinical experiences and genetic results in six patients.Small proportion of CVID patients are also PLAID/APLAID/FCAS3 patients and all these have disease-causing-mutations in PLCG2-genes,so it may be better to define all of them as “PLCG2 deficiency”. Key Clinical Message: Germline mutations in PLCG2 gene cause PLAID,APLAID,FCAS3, and CVID.Clinical experiences in patients with PLCG2 mutations led us to consider that PLAID, APLAID and FCAS3 are same diseases.It may be better to define all of them as “PLCG2 deficiency”. INTRODUCTION The PLCG2 gene which is located on the 16th chromosome (16q23.3) encodes phospholipase Cg2 (PLCG2), a transmembrane signaling enzyme that catalyzes the production of second messenger molecules utilizing calcium as a cofactor and propagates downstream signals in several hematopoietic cells (1). Recently, het- erozygous germline mutations in human PLCG2 were linked to some clinical phenotypes with some overlap- ping features|PLCg2-associated antibody deficiency and immune dysregulation syndrome (PLAID) (OMIM 614878) and autoinflammation, antibody deficiency, and immune dysregulation syndrome (APLAID) (OMIM 614878) (2-4) and familial cold autoinflammatory syndrome (FCAS3) (OMIM 614468) (5). All of them are autosomal dominant inherited diseases. -
Open Access for Incredible Lupus Research
Lupus: Open Access Editorial Note Lupus: Open Access for Incredible Lupus Research Yves Renaudineau* Immunotherapy Graft Oncology, Innovative Medicines initiative precisesads, Réseau épigénétique et réseau canaux ioniques du Cancéropole Grand Ouest, European University of Brittany, Brest, France EDITOR’S PICKS The 04th Volume of this esteemed journal addresses the novel research performed by authors from parts of the world. Lupus is an Incurable auto immune disorder in which body Weinmann-Menke J, et al. in their case reports discusses that immune system attacks its own tissues or organs. It affects many Since our patient is suffering from the autoimmune disease parts of the body including Skin (Subcutaneous/cutaneous lupus erythematodes and is listed for kidney transplantation due Lupus), Kidneys (Lupus Nephrites), Brain (Cerebral/CNS to end stage renal disease, it is very likely that Lupus) etc., with several symptoms of Rashes (Malar, Discoid or immunosuppressant therapy will have to be initiated again in the photosensitive), Musculoskeletal Problems, Serositis, Anemia, future [1]. Seziures and several many more. We can find several Diagnostic approaches for Lupus. Elagib EM, et al. in his research article discloses that It is important to identify the possible differences in the effectiveness There is no cure for lupus, Yet many treatment options includes of rituximab in treating patients of CAPS associated with SLE NSAIDS, Immunosuoressives, Malario therapy, Usage of and patients of primary CAPS in order to determine the possible Steroids along with life style modifications and healthy diet can prognostic factors that could affect the therapeutic decisions and reduce the risk of lupus effected patients. The statistics provided results [2]. -
Innate Immunity in the Lung: How Epithelial Cells Fight Against
Copyright #ERSJournals Ltd 2004 EurRespir J 2004;23: 327– 333 EuropeanRespiratory Journal DOI: 10.1183/09031936.03.00098803 ISSN0903-1936 Printedin UK –allrights reserved REVIEW Innateimmunity in the lung: how epithelialcells ght against respiratorypathogens R. Bals*,P.S. Hiemstra # Innateimmunity in the lung: how epithelial cells ® ghtagainst respiratory pathogens *Deptof Internal Medicine, Division of R Bals, P S Hiemstra #ERS JournalsLtd 2004 PulmonaryMedicine, Hospital of the Uni- versityof Marburg, Philipps-University, ABSTRACT: Thehuman lung is exposed to a largenumber of airborne pathogens as a # resultof the daily inhalation of 10,000 litres of air Theobservation that respiratory Marburg,Germany; Deptof Pulmonology, LeidenUniversity Medical Center, Leiden, infectionsare nevertheless rare is testimony to the presence of anef®cient host defence TheNetherlands systemat the mucosal surface of the lung Theairway epithelium is strategically positioned at the interface with the Correspondence:P S Hiemstra,Dept of environment,and thus plays a keyrole in this host defence system Recognition Pulmonology,Leiden University Medical systemsemployed by airwayepithelial cells to respond to microbialexposure include the Center, P O Box9600, 2300 RC Leiden, The actionof the toll-like receptors Netherlands Theairway epithelium responds to such exposure by increasing its production of Fax:31 715266927 mediatorssuch as cytokines, chemokines and antimicrobial peptides Recent® ndings E-mail: p s hiemstra@lumc nl indicatethe importance of these peptides -
Immune Disorder
EDITORIAL Immune disorder Dr.Dingliang Lv* EDITORIAL vaccines and antiseptics, kids today aren’t exposed to as many germs as they were at intervals the past. The shortage of exposure might produce their Immune Disorder could also be a condition at intervals that your system system liable to react to harmless substances. mistakenly attacks your body. The system guards against germs like bacteria and viruses. Once it senses these foreign invaders, it sends out a military of The early symptoms of the many response diseases square measure terribly fighter cells to attack them. In degree illness, the system mistakes a section similar, such as: Fatigue, aching muscles, Swelling and redness, inferior of your body, like your joints or skin, as foreign. It releases proteins fever, bother concentrating, symptom and tingling within the hands and mentioned as auto antibodies that attack healthy cells. Some reaction feet, Hair loss, Skin rashes. diseases target only 1 organ. The system can tell the excellence between Individual diseases may also have their own distinctive symptoms. For foreign cells and your own cells. instance, kind one polygenic disorder causes extreme thirst, weight loss, and Immune System Attack the body because of the following reasons however fatigue. IBD causes belly pain, bloating, and looseness of the bowels. With some people square Measure plenty of probably to induce degree illness response diseases like skin condition or RA, symptoms might return and go. than others. In step with a 2014 study, girls get reaction diseases at a rate of An amount of symptoms is termed outburst. An amount once the regarding 2 to 1 compared to men-half-dozen.4 proportion of women vs. -
Hypersensitivity in General Immune System Is Protective in Nature by Protecting Host Body from Harmful and Infectious Foreign Microorganisms
Hypersensitivity In general immune system is protective in nature by protecting host body from harmful and infectious foreign microorganisms. But hypersensitivity is an immune disorder where immune system responds more than required and cause harmful effects in host. Hypersensitivity is defined as an exaggeration immune response that results in tissue damage in a sensitized individual on 2nd or subsequent contact with specific antigens. This condition is also called allergy. The first contact with an antigen leads to sensitization the immune system in the host for production of specific allergen produces the manifestation of hypersensitivity. This is known as shocking dose. Basing on the time required for the appearance of the hypersensitivity reactions. They are classified into two types: 1. Immediate hypersensitivity 2. Delayed hypersensitivity Peter Gell and Robert Coombs classified hypersensitivity reactions into 4 types based on the mechanism of pathogenesis: Type 1: IgE mediated hypersensitivity Type 2: Ab dependent cytotoxic hypersensitivity Type 3: Immune complex mediated hypersensitivity Type 4: Cell mediated delayed hypersensitivity The first three types of hypersensitivity reactions are mediated through the production of Antibodies and the fourth type of reaction is mediated through the production of T cells. Type 1: IgE mediated hypersensitivity It occurs in two forms anaphylaxis and atopy. i. Anaphylaxis It is an acute, fatal and systemic form of type I hypersensitivity. The allergens include antibiotics like Penicillin, antitoxin, insect venom etc. On first contact with allergen and lymphocytes are differentiated into plasma cells and produce specific Immunoglobulin IgE also called as ''Reagin antibodies'' which binds to the Fc receptors of mast cells or basophiles and sensitizes these cells that make the individual allergic to the antigen. -
Hypersensitivity Adverse Event Reporting in Clinical Cancer Trials: Barriers and Potential Solutions to Studying Severe Events on a Population Level
University of Wisconsin Milwaukee UWM Digital Commons Theses and Dissertations May 2020 Hypersensitivity Adverse Event Reporting in Clinical Cancer Trials: Barriers and Potential Solutions to Studying Severe Events on a Population Level Christina E. Eldredge University of Wisconsin-Milwaukee Follow this and additional works at: https://dc.uwm.edu/etd Part of the Library and Information Science Commons, and the Medicine and Health Sciences Commons Recommended Citation Eldredge, Christina E., "Hypersensitivity Adverse Event Reporting in Clinical Cancer Trials: Barriers and Potential Solutions to Studying Severe Events on a Population Level" (2020). Theses and Dissertations. 2371. https://dc.uwm.edu/etd/2371 This Dissertation is brought to you for free and open access by UWM Digital Commons. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of UWM Digital Commons. For more information, please contact [email protected]. HYPERSENSITIVITY ADVERSE EVENT REPORTING IN CLINICAL CANCER TRIALS: BARRIERS AND POTENTIAL SOLUTIONS TO STUDYING SEVERE EVENTS ON A POPULATION LEVEL by Christina Eldredge A Dissertation Submitted in Partial Fulfillment of the Requirements for the Degree of Doctor in Philosophy in Biomedical and Health Informatics at The University of Wisconsin-Milwaukee May 2020 ABSTRACT HYPERSENSITIVITY ADVERSE EVENT REPORTING IN CLINICAL CANCER TRIALS: BARRIERS AND POTENTIAL SOLUTIONS TO STUDYING ALLERGIC EVENTS ON A POPULATION LEVEL by Christina Eldredge The University of Wisconsin-Milwaukee, 2020 Under the Supervision of Professor Timothy Patrick Clinical cancer trial interventions are associated with hypersensitivity events (HEs) which are recorded in the national clinical trial registry, ClinicalTrials.gov and publicly available. This data could potentially be leveraged to study predictors for HEs to identify at risk patients who may benefit from desensitization therapies to prevent these potentially life-threatening reactions. -
Qnas with Max D. Cooper and Jacques F. A. P. Miller
QNAS QnAswithMaxD.CooperandJacquesF.A.P.Miller QNAS Brian Doctrow, Science Writer Anyone who has ever contracted chicken pox can thank the adaptive immune system for future pro- tection against the disease. It is also thanks to this system that vaccines prevent diseases. The adaptive immune system provides organisms with a memory of past infections, enabling the body to quickly kill returning infections before they can do significant damage. Immunologists Jacques F. A. P. Miller and Max D. Cooper determined that adaptive immunity requires 2 distinct cell types that perform comple- mentary functions. Miller’s findings, published in the early 1960s in Lancet (1) and Proceedings of the Royal Society (2), showed that the ability to distinguish one’s own cells from foreign cells, a key feature of the adap- tive immune system, depends on lymphocytes, now known as T cells, matured in an organ called the thy- mus. Subsequently, Cooper reported in Nature (3) that Max Dale Cooper. Image courtesy of Georgia Research antibody production depends on a separate set of Alliance/Billy Howard. lymphocytes, dubbed B cells. The division of labor between T and B cells is a fundamental organizing principle of the adaptive immune system, the discov- did cancer research. I started working on leukemia and ery of which laid the groundwork for modern immu- this gave me an interest in lymphocytes. nology and made possible many subsequent medical advances, including monoclonal antibody produc- Cooper: I became interested through patients that I tion, vaccine development, and checkpoint inhibi- was taking care of: Children that had deficient immune tion therapies for cancer. -
The Role of Microbiota in the Pathogenesis of Esophageal Adenocarcinoma
biology Review The Role of Microbiota in the Pathogenesis of Esophageal Adenocarcinoma Megan R. Gillespie 1, Vikrant Rai 2 , Swati Agrawal 3 and Kalyana C. Nandipati 3,* 1 School of Medicine, Creighton University, 2500 California Plaza, Omaha, NE 68178, USA; [email protected] 2 Department of Translational Research, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA 91766, USA; [email protected] 3 Department of Surgery, Creighton University School of Medicine, 2500 California Plaza, Omaha, NE 68178, USA; [email protected] * Correspondence: [email protected]; Tel.: +1-402-280-5292 Simple Summary: Esophageal adenocarcinoma has a poor 5-year survival rate and is among the highest mortality cancers. Changes in the esophageal microbiome have been associated with cancer pathogenesis; however, the molecular mechanism remains obscure. This review article critically analyzes the molecular mechanisms through which microbiota may mediate the development and progression of esophageal adenocarcinoma and its precursors-gastroesophageal reflux disease and Barrett’s esophagus. It summarizes changes in esophageal microbiome composition in normal and pathologic states and subsequently discusses the role of altered microbiota in disease progression. The potential role of esophageal microbiota in protecting against the development of esophageal adenocarcinoma is also discussed. By doing so, this article highlights specific directions for future research developing microbiome-mediated therapeutics for esophageal adenocarcinoma. Abstract: Esophageal adenocarcinoma (EAC) is associated with poor overall five-year survival. The Citation: Gillespie, M.R.; Rai, V.; incidence of esophageal cancer is on the rise, especially in Western societies, and the pathophysiologic Agrawal, S.; Nandipati, K.C. The Role of Microbiota in the Pathogenesis of mechanisms by which EAC develops are of extreme interest. -
Human Autoimmunity and Associated Diseases
Human Autoimmunity and Associated Diseases Human Autoimmunity and Associated Diseases Edited by Kenan Demir and Selim Görgün Human Autoimmunity and Associated Diseases Edited by Kenan Demir and Selim Görgün This book first published 2021 Cambridge Scholars Publishing Lady Stephenson Library, Newcastle upon Tyne, NE6 2PA, UK British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Copyright © 2021 by Kenan Demir and Selim Görgün and contributors All rights for this book reserved. No part of this book may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission of the copyright owner. ISBN (10): 1-5275-6910-1 ISBN (13): 978-1-5275-6910-2 TABLE OF CONTENTS Preface ...................................................................................................... viii Chapter One ................................................................................................. 1 Introduction to the Immune System Kemal Bilgin Chapter Two .............................................................................................. 10 Immune System Embryology Rümeysa Göç Chapter Three ............................................................................................. 18 Immune System Histology Filiz Yılmaz Chapter Four .............................................................................................. 36 Tolerance Mechanisms and Autoimmunity -
Immunology 101
Immunology 101 Justin Kline, M.D. Assistant Professor of Medicine Section of Hematology/Oncology Committee on Immunology University of Chicago Medicine Disclosures • I served as a consultant on Advisory Boards for Merck and Seattle Genetics. • I will discuss non-FDA-approved therapies for cancer 2 Outline • Innate and adaptive immune systems – brief intro • How immune responses against cancer are generated • Cancer antigens in the era of cancer exome sequencing • Dendritic cells • T cells • Cancer immune evasion • Cancer immunotherapies – brief intro 3 The immune system • Evolved to provide protection against invasive pathogens • Consists of a variety of cells and proteins whose purpose is to generate immune responses against micro-organisms • The immune system is “educated” to attack foreign invaders, but at the same time, leave healthy, self-tissues unharmed • The immune system can sometimes recognize and kill cancer cells • 2 main branches • Innate immune system – Initial responders • Adaptive immune system – Tailored attack 4 The immune system – a division of labor Innate immune system • Initial recognition of non-self (i.e. infection, cancer) • Comprised of cells (granulocytes, monocytes, dendritic cells and NK cells) and proteins (complement) • Recognizes non-self via receptors that “see” microbial structures (cell wall components, DNA, RNA) • Pattern recognition receptors (PRRs) • Necessary for priming adaptive immune responses 5 The immune system – a division of labor Adaptive immune system • Provides nearly unlimited diversity of receptors to protect the host from infection • B cells and T cells • Have unique receptors generated during development • B cells produce antibodies which help fight infection • T cells patrol for infected or cancerous cells • Recognize “foreign” or abnormal proteins on the cell surface • 100,000,000 unique T cells are present in all of us • Retains “memory” against infections and in some cases, cancer.