Antigens & Antibodies II Polyclonal Antibodies Vs Monoclonal Antibodies
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Antigen –Antibody Interaction By: Dr
TDC 5TH SEM MAJOR: PAPER 5.3 ANTIGEN –ANTIBODY INTERACTION BY: DR. LUNA PHUKAN Antigen-antibody interaction, or antigen-antibody reaction, is a specific chemical interaction between antibodies produced by B cells of the white blood cells and antigens during immune reaction. The antigens and antibodies combine by a process called agglutination Antigen-antibody interaction, or antigen-antibody reaction, is a specific chemical interaction between antibodies produced by B cells of the white blood cells and antigens during immune reaction. The antigens and antibodies combine by a process called agglutination. It is the fundamental reaction in the body by which the body is protected from complex foreign molecules, such as pathogens and their chemical toxins. In the blood, the antigens are specifically and with high affinity bound by antibodies to form an antigen- antibody complex. The immune complex is then transported to cellular systems where it can be destroyed or deactivated. The first correct description of the antigen-antibody reaction was given by Richard J. Goldberg at the University of Wisconsin in 1952. It came to be known as "Goldberg's theory" (of antigen-antibody reaction) There are several types of antibodies and antigens, and each antibody is capable of binding only to a specific antigen. The specificity of the binding is due to specific chemical constitution of each antibody. The antigenic determinant or epitope is recognized by the paratope of the antibody, situated at the variable region of the polypeptide chain. The variable region in turn has hyper-variable regions which are unique amino acid sequences in each antibody. -
Ch. 43 the Immune System
Ch. 43 The Immune System 1 Essential Questions: How does our immunity arise? How does our immune system work? 2 Overview of immunity: Two kinds of defense: A. innate immunity present at time of birth before exposed to pathogens nonspecific responses, broad in range skin and mucous membranes internal cellular and chemical defenses that get through skin macrophages, phagocytic cells B. acquired immunity (adaptive immunity)develops after exposure to specific microbes, abnormal body cells, foreign substances or toxins highly specific lymphocytes produce antibodies or directly destroy cells 3 Overview of Immune System nonspecific Specific 4 I. Innate immunity Nonspecific defenses A. First line of defense: skin, mucous membranes skin protects against chemical, mechanical, pathogenic, UV light damage mucous membranes line digestive, respiratory, and genitourinary tracts prevent pathogens by trapping in mucus *breaks in skin or mucous membranes = entryway for pathogen 5 secretions of skin also protect against microbes sebaceous and sweat glands keep pH at 35 stomach also secretes HCl (Hepatitis A virus can get past this) produce antimicrobial proteins (lysozyme) ex. in tears http://vrc.belfastinstitute.ac.uk/resources/skin/skin.htm 6 B. Second line of defense internal cellular and chemical defenses (still nonspecific) phagocytes produce antimicrobial proteins and initiate inflammation (helps limit spread of microbes) bind to receptor sites on microbe, then engulfs microbe, which fused with lysosome nitric oxide and poisons in lysosome can poison microbe lysozyme and other enzymes degrade the microbe *some bacteria have capsule that prevents attachment *some bacteria are resistant to lysozyme macrophages 7 Cellular Innate defenses Tolllike receptor (TLR) recognize fragments of molecules characteristic of a set of pathogens [Ex. -
The RAG Recombinase Dictates Functional Heterogeneity and Cellular Fitness in Natural Killer Cells
The RAG Recombinase Dictates Functional Heterogeneity and Cellular Fitness in Natural Killer Cells Jenny M. Karo,1 David G. Schatz,2 and Joseph C. Sun1,* 1Immunology Program and Gerstner Sloan Kettering Graduate School of Biomedical Sciences, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA 2Department of Immunobiology and the Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510, USA *Correspondence: [email protected] http://dx.doi.org/10.1016/j.cell.2014.08.026 SUMMARY completely absent (Mombaerts et al., 1992; Shinkai et al., 1992). There is as yet no evidence that RAG plays a physiological The emergence of recombination-activating genes role in any cell type other than B and T lymphocytes or in any pro- (RAGs) in jawed vertebrates endowed adaptive cess other than V(D)J recombination. immune cells with the ability to assemble a diverse Although NK cells have long been classified as a component set of antigen receptor genes. In contrast, innate of the innate immune system, recent evidence suggests that lymphocytes, such as natural killer (NK) cells, are this cell type possesses traits attributable to adaptive immunity not believed to require RAGs. Here, we report that (Sun and Lanier, 2011). These characteristics include ‘‘educa- tion’’ mechanisms to ensure self-tolerance during NK cell devel- NK cells unable to express RAGs or RAG endonu- opment and clonal-like expansion of antigen-specific NK clease activity during ontogeny exhibit a cell-intrinsic cells during viral infection, followed by the ability to generate hyperresponsiveness but a diminished capacity long-lived ‘‘memory’’ NK cells. -
Perspectives on in Vitro Diagnostic Devices, Regulated by the Office Of
1 2 “This transcript appears as received from the commercial transcribing service after inclusion of minor corrections to typographical and factual errors recommended by the Technical Point of Contact.” 1 PERSPECTIVES ON IN VITRO DIAGNOSTIC DEVICES, 2 REGULATED BY THE OFFICE OF BLOOD RESEARCH AND REVIEW 3 4 FOOD AND DRUG ADMINISTRATION 5 WHITE OAK CAMPUS 6 BUILDING 31 7 10903 NEW HAMPSHIRE AVENUE 8 SILVER SPRING, MARYLAND 20903 9 10 TUESDAY, JULY 16, 2019 11 8:30 A.M. 12 13 APPEARANCES: 14 MODERATOR: TERESITA C. MERCADO, MS 15 16 WELCOME: 17 JULIA LATHROP, PHD, DETTD/OBRR 18 19 INTRODUCTION: 20 WENDY PAUL, MD, DBCD/OBRR 21 22 PRESENTERS: 23 KIMBERLY BIGLER, MLS(ASCP)CMSBB, DBCD/OBRR 1 ANNETTE RAGOSTA, MT(ASCP)SBB, DBCD/OBRR 2 ZHUGONG "JASON" LIU, PHD, DRB/DBCD 3 4 CONFERENCE 5 TUESDAY, JULY 16, 2019 6 8:30 A.M. 7 DR. LATHROP: Okay, everybody. Thank you for coming to the second day of 8 our workshop which is going to be focused on considerations for IVDs regulated by the Division 9 of Blood Components and Devices in OBRR. 10 Again, the slides will be available on the website in about two weeks, so take a 11 look for them there. And moderating today’s session is Teresita Mercado from the Division. 12 MS. MERCADO: Good morning. Welcome to session three of the IVD 13 workshop. Our first speaker will be Dr. Wendy Paul. She is the deputy director of DBCD who 14 will give us an introduction to devices in DBCD. 15 DR. -
LECTURE 05 Acquired Immunity and Clonal Selection
LECTURE: 05 Title: ACQUIRED "ADAPTIVE" IMMUNITY & CLONAL SELECTION THEROY LEARNING OBJECTIVES: The student should be able to: • Recognize that, acquired or adaptive immunity is a specific immunity. • Explain the mechanism of development of the specific immunity. • Enumerate the components of the specific immunity such as A. Primary immune response. B. Secondary immune response • Explain the different phases that are included in the primary and secondary immune responses such as: A. The induction phase. B. Exponential phase. C. Steady phase. D. Decline phase. • Compare between the phases of the primary and secondary immune responses. • Determine the type of the immunoglobulins involved in each phase. • Determine which immunoglobulin is induced first and, that last longer. • Enumerate the characteristics of the specific immunity such as: A. The ability to distinguish self from non-self. B. Specificity. C. Immunological memory. • Explain naturally and artificially acquired immunity (passive, and active). • Explain the two interrelated and independent mechanisms of the specific immune response such as : A. Humoral immunity. B. Cell-mediated (cellular) immunity. • Recognize that, the specific immunity is not always protective, for example; sometimes it causes allergies (hay fever), or it may be directed against one of the body’s own constituents, resulting in autoimmunity (thyroditis). LECTURE REFRENCE: 1. TEXTBOOK: ROITT, BROSTOFF, MALE IMMUNOLOGY. 6th edition. Chapter 2. pp. 15-31 2. TEXTBOOK: ABUL K. ABBAS. ANDREW H. LICHTMAN. CELLULAR AND MOLECULAR IMMUNOLOGY. 5TH EDITION. Chapter 1. pg 3-12. 1 ACQUIRED (SPECIFIC) IMMUNITY INTRODUCTION Adaptive immunity is created after an interaction of lymphocytes with particular foreign substances which are recognized specifically by those lymphocytes. -
Med-Pathway Zoom Workshop
MCAT Immunology Dr. Phillip Carpenter medpathwaymcat Med-pathway AAMC MCAT Content Outline: Immunology Category 1A: Structure/Function of Proteins/AA Immune System Category 3B: Organ Systems Innate vs. Adaptive Immunity T and B Lymphocytes Macrophages & Phagocytes Tissue-Bone marrow, Spleen, Thymus, Lymph nodes Antigen and Antibody Antigen Presentation Clonal Selection Antigen-Antibody recognition Structure of antibody molecule Self vs. Non-self, Autoimmune Diseases Major Histocompatibility Complex Lab Techniques: ELISA & Western Blotting Hematopoiesis Creates Immune Cells Self vs. Non-self Innate vs Adaptive Innate Immunity Physical Barriers: Skin, mucous membranes, pH Inflammatory mediators: Complement, Cytokines, Prostaglandins Cellular Components: Phagocytes-Neutrophils, Eosinophils, Basophils, Mast Cells Antigen Presenting Cells-Monocytes, Macrophages, Dendritic Cells Adaptive (Acquired) Immunity Composed of B and T lymphocytes: Activated by Innate Immunity B cells: Express B cell receptor and secrete antibodies as plasma cells T cells: Mature in thymus, express TCR surface receptor; Activated by Antigen Presenting Cells (APCs) Direct Immune response (The Ringleaders of immune system) Major Lymphoid Organs TYPE SITE FUNCTION Fetal production of Liver 1° lymphoid cells Hematopoietic production of 1° Bone marrow myeloid and lymphoid cells Receives bone marrow T 1° Thymus cells; site where self is selected from non-self Lymph nodes 2° Sites of antigen activation Spleen of lymphocytes; clearance Macrophages (Sentinel Cells) Pattern Recognition -
Subdominant CD8 T-Cell Epitopes Account for Protection Against Cytomegalovirus Independent of Immunodominationᰔ† Rafaela Holtappels,1* Christian O
JOURNAL OF VIROLOGY, June 2008, p. 5781–5796 Vol. 82, No. 12 0022-538X/08/$08.00ϩ0 doi:10.1128/JVI.00155-08 Copyright © 2008, American Society for Microbiology. All Rights Reserved. Subdominant CD8 T-Cell Epitopes Account for Protection against Cytomegalovirus Independent of Immunodominationᰔ† Rafaela Holtappels,1* Christian O. Simon,1 Michael W. Munks,2‡ Doris Thomas,1 Petra Deegen,1 Birgit Ku¨hnapfel,1 Torsten Da¨ubner,1 Simone F. Emde,1 Ju¨rgen Podlech,1 Natascha K. A. Grzimek,1 Silke A. Oehrlein-Karpi,1 Ann B. Hill,2 and Matthias J. Reddehase1 Institute for Virology, Johannes Gutenberg University, 55131 Mainz, Germany,1 and Department of Molecular Microbiology and Immunology, Oregon Health and Science University, Portland, Oregon 972392 Received 22 January 2008/Accepted 17 March 2008 Cytomegalovirus (CMV) infection continues to be a complication in recipients of hematopoietic stem cell transplantation (HSCT). Preexisting donor immunity is recognized as a favorable prognostic factor for the reconstitution of protective antiviral immunity mediated primarily by CD8 T cells. Furthermore, adoptive transfer of CMV-specific memory CD8 T (CD8-TM) cells is a therapeutic option for preventing CMV disease in HSCT recipients. Given the different CMV infection histories of donor and recipient, a problem may arise from an antigenic mismatch between the CMV variant that has primed donor immunity and the CMV variant acquired by the recipient. Here, we have used the BALB/c mouse model of CMV infection in the immunocom- promised host to evaluate the importance of donor-recipient CMV matching in immundominant epitopes (IDEs). For this, we generated the murine CMV (mCMV) recombinant virus mCMV-⌬IDE, in which the two memory repertoire IDEs, the IE1-derived peptide 168-YPHFMPTNL-176 presented by the major histocom- patibility complex class I (MHC-I) molecule Ld and the m164-derived peptide 257-AGPPRYSRI-265 presented d by the MHC-I molecule D , are both functionally deleted. -
PLATELIA™ TOXO Igg AVIDITY 72842
PLATELIA™ TOXO IgG AVIDITY 48 72842 DETERMINATION OF ANTI-TOXOPLASMA GONDII IgG AVIDITY IN HUMAN SERUM BY ENZYME IMMUNOASSAY 881130 - 2013/11 Table of Content 1- INTENDED USE ...............................................................................3 2- CLINICAL VALUE ............................................................................3 3- PRINCIPLE ......................................................................................4 4- PRODUCT INFORMATION ..............................................................5 5- WARNINGS AND PRECAUTIONS ..................................................5 6- SAMPLES ........................................................................................7 7- ASSAY PROCEDURE ......................................................................7 8- INTERPRETATION OF RESULTS .................................................10 9- PERFORMANCES .........................................................................11 10- LIMITATIONS OF THE PROCEDURE ...........................................13 11- QUALITY CONTROL OF THE MANUFACTURER .........................13 12- REFERENCES ...............................................................................14 2 [EN] 1. INTENDED USE Platelia™ TOXO IgG AVIDITY is an immuno-enzyme assay for determination of avidity of anti-T. gondii IgG antibodies in human serum. The Platelia™ TOXO IgG AVIDITY assay should be used in association with the Platelia™ TOXO IgG kit (Ref. 72840). 2. CLINICAL VALUE T. gondii is a protozoan causing infection in numerous -
Monoclonal Antibodies As Tools to Combat Fungal Infections
Journal of Fungi Review Monoclonal Antibodies as Tools to Combat Fungal Infections Sebastian Ulrich and Frank Ebel * Institute for Infectious Diseases and Zoonoses, Faculty of Veterinary Medicine, Ludwig-Maximilians-University, D-80539 Munich, Germany; [email protected] * Correspondence: [email protected] Received: 26 November 2019; Accepted: 31 January 2020; Published: 4 February 2020 Abstract: Antibodies represent an important element in the adaptive immune response and a major tool to eliminate microbial pathogens. For many bacterial and viral infections, efficient vaccines exist, but not for fungal pathogens. For a long time, antibodies have been assumed to be of minor importance for a successful clearance of fungal infections; however this perception has been challenged by a large number of studies over the last three decades. In this review, we focus on the potential therapeutic and prophylactic use of monoclonal antibodies. Since systemic mycoses normally occur in severely immunocompromised patients, a passive immunization using monoclonal antibodies is a promising approach to directly attack the fungal pathogen and/or to activate and strengthen the residual antifungal immune response in these patients. Keywords: monoclonal antibodies; invasive fungal infections; therapy; prophylaxis; opsonization 1. Introduction Fungal pathogens represent a major threat for immunocompromised individuals [1]. Mortality rates associated with deep mycoses are generally high, reflecting shortcomings in diagnostics as well as limited and often insufficient treatment options. Apart from the development of novel antifungal agents, it is a promising approach to activate antimicrobial mechanisms employed by the immune system to eliminate microbial intruders. Antibodies represent a major tool to mark and combat microbes. Moreover, monoclonal antibodies (mAbs) are highly specific reagents that opened new avenues for the treatment of cancer and other diseases. -
Enzyme Immunoassays for the Diagnostics of Toxoplasmosis
INFECTIOUS SEROLOGY – PARASITOLOGY – Toxoplasma gondii FOLLOW US FOLLOW US Toxoplasma gondii Enzyme immunoassays for the diagnostics of toxoplasmosis ELISA and IMMUNOBLOT kits are optimized and validated for detection of IgA, IgE, IgG and IgM antibodies in human serum and plasma BIOVENDOR.GROUP INFECTIOUS SEROLOGY – PARASITOLOGY – Toxoplasma gondii Introduction Diagnosis of infection Toxoplasmosis is a widespread parasitic disease cau- Diagnosis of the disease is based on epidemiological sed by protozoan Toxoplasma gondii – a parasite with anamnesis, clinical manifestation and laboratory tests. a complicated life cycle consisting of several morpho- Direct detection of the parasite is not available for rou- logically different stadia. Primary hosts are members of tine diagnostics. Serology is the most important tool for the feline family. Humans and most warm-blooded ani- laboratory diagnostics of toxoplasmosis. mals can be infected by either primarily infected food – Screening – determination of total antibodies by (insufficiently heat-treated meat) or by ingestion of oo- complement fixation test (CFT) cysts (secondary contaminated food or contaminated – Determination of specific IgA, IgE, IgM, IgG fingers, objects, etc.). antibodies and IgG avidity by ELISA and confirmation Acquired toxoplasmosis in immunocompetent indi- of results by Immunoblot viduals is usually asymptomatic or can manifest itself with flu-like symptoms (subfebrility, fatigue, lymphade- nopathy, muscle aches) and has no lasting ill effects. Severe life-threatening infections (encephalitis, hepati- tis, chorioretinitis, myocarditis, generalized form of the disease) may develop in immunocompromised patients usually because of a reactivation of a latent infection. Congenital toxoplasmosis is caused by transmission of infection from mother to foetus and it might result in severe damages of the foetus (brain calcification, hydrocepha- lus, vision disorders, mental affections), still birth or abortion. -
Clinical Significance of Igg Avidity Testing and Other
medical sciences Review Clinical Significance of IgG Avidity Testing and Other Considerations in the Diagnosis of Congenital Cytomegalovirus Infection: A Review Update Idris Abdullahi Nasir 1,2,*, Adamu Babayo 3 and Muhammad Sagir Shehu 4 1 Department of Medical Laboratory Services, University of Abuja Teaching Hospital, Gwagwalada, FCT Abuja PMB 228, Nigeria 2 Department of Medical Microbiology and Parasitology, College of Health Sciences, University of Ilorin, PMB 1515 Ilorin, Nigeria 3 Department of Medical Microbiology, Abubakar Tafawa Balewa University Teaching Hospital, Bauchi PMB 0117, Nigeria; [email protected] 4 Immunology unit, Department of Medicine, Ahmadu Bello University, PMB 05 Zaria, Kaduna State, Nigeria; [email protected] * Correspondence: [email protected]; Tel.: +234-8030522324; Fax: +234-8055982223 Academic Editor: Hung-Yun Lin Received: 24 November 2015; Accepted: 3 March 2016; Published: 8 March 2016 Abstract: Prompt and accurate laboratory testing of women before or during antenatal days is necessary for detecting humoral immunological responses against cytomegalovirus (CMV) infection and assessing risk of congenital transmission. CMV is the most common viral etiology with the greatest propensity to induce neonatal pathologies. Most healthcare facilities in developing countries rely solely on anti-CMV IgM and IgG assays in diagnosing CMV infections. However, these parameters have some worrisome limitations. This study reviewed the significance of IgG avidity testing as a highly sensitive and specific tool that improves decisions regarding diagnosis of maternal and congenital CMV infections. We conducted this review from relevant published articles using an extensive literature search made through PubMed, Scopus and Google scholar on the concepts of congenital CMV (CCMV) transmission and clinical significance of IgG avidity testing in diagnosis of CCMV infections. -
Theories of Antibodies Production
THEORIES OF ANTIBODIES PRODUCTION 1. Instructive Theories a. Direct Template Theory b. Indirect Template Theory 2. Selective Theories a. Natural Selection Theory b. Side Chain Theory c. Clonal Selection Theory d. Immune Network Theory INSTRUCTIVE THEORIES Instructive theories suggest that an immunocompetent cell is capable of synthesizing antibodies of all specificity. The antigen directs the immunocompetent cell to produce complementary antibodies. According to these theories the antigen play a central role in determining the specificity of antibody molecule. Two instructive theories are postulated as follows: Direct template theory: This theory was first postulated by Breinl and Haurowitz (1930). They suggested that a particular antigen or antigenic determinants would serve as a template against which antibodies would fold. The antibody molecule would thereby assume a configuration complementary to antigen template. This theory was further advanced as Direct Template Theory by Linus Pauling in 1940s. Indirect template theory: This theory was first postulated by Burnet and Fenner (1949). They suggested that the entry of antigenic determinants into the antibody producing cells induced a heritable change in these cells. A genocopy of the antigenic determinant was incorporated in genome of these cells and transmitted to the progeny cells. However, this theory that tried to explain specificity and secondary responses is no longer accepted. SELECTIVE THEORIES Selective theories suggest that it is not antigen, but the antibody molecule that play a central role in determining its specificity. The immune system already possess pre-formed antibodies of different specificities prior to encounter with an antigen. Three selective theories were postulated as follows: Side chain theory: This theory was proposed by Ehrlich (1898).