MICR 5051 Introduction to Immunology FALL 2015
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Spontaneous Reversal of Acquired Autoimmune Dysfibrinogenemia Probably Due to an Antiidiotypic Antibody Directed to an Interspec
Spontaneous reversal of acquired autoimmune dysfibrinogenemia probably due to an antiidiotypic antibody directed to an interspecies cross-reactive idiotype expressed on antifibrinogen antibodies. A Ruiz-Arguelles J Clin Invest. 1988;82(3):958-963. https://doi.org/10.1172/JCI113704. Research Article A young man with a long history of abnormal bleeding was seen in January 1985. Coagulation tests showed dysfibrinogenemia and an antifibrinogen autoantibody was demonstrable in his serum. This antibody, when purified, was capable of inhibiting the polymerization of normal fibrin monomers, apparently through binding to the alpha fibrinogen chain. 6 mo later the patient was asymptomatic, coagulation tests were normal, and the antifibrinogen autoantibody was barely detectable. At this time, affinity-purified autologous and rabbit antifibrinogen antibodies were capable of absorbing an IgG kappa antibody from the patient's serum, which reacted indistinctly with both autologous and xenogeneic antifibrinogen antibodies in enzyme immunoassays. It has been concluded that the patient's dysfibrinogenemia was the result of an antifibrinogen autoantibody, and that later on an anti-idiotype antibody, which binds an interspecies cross- reactive idiotype expressed on anti-human fibrinogen antibodies, inhibited the production of the antifibrinogen autoantibody which led to the remission of the disorder. Find the latest version: https://jci.me/113704/pdf Spontaneous Reversal of Acquired Autoimmune Dysfibrinogenemia Probably Due to an Antildiotypic Antibody Directed to an Interspecies Cross-reactive Idiotype Expressed on Antifibrinogen Antibodies Alejandro Ruiz-Arguelles Department ofImmunology, Laboratorios Clinicos de Puebla, Puebla, Puebla 72530, Mexico Abstract disorder. This anti-Id antibody was shown to react with xeno- geneic antifibrinogen antibodies, hence, its specificity is an A young man with a long history of abnormal bleeding was interspecies cross-reactive Id (IdX)' most likely encoded by seen in January 1985. -
Our Immune System (Children's Book)
OurOur ImmuneImmune SystemSystem A story for children with primary immunodeficiency diseases Written by IMMUNE DEFICIENCY Sara LeBien FOUNDATION A note from the author The purpose of this book is to help young children who are immune deficient to better understand their immune system. What is a “B-cell,” a “T-cell,” an “immunoglobulin” or “IgG”? They hear doctors use these words, but what do they mean? With cheerful illustrations, Our Immune System explains how a normal immune system works and what treatments may be necessary when the system is deficient. In this second edition, a description of a new treatment has been included. I hope this book will enable these children and their families to explore together the immune system, and that it will help alleviate any confusion or fears they may have. Sara LeBien This book contains general medical information which cannot be applied safely to any individual case. Medical knowledge and practice can change rapidly. Therefore, this book should not be used as a substitute for professional medical advice. SECOND EDITION COPYRIGHT 1990, 2007 IMMUNE DEFICIENCY FOUNDATION Copyright 2007 by Immune Deficiency Foundation, USA. Readers may redistribute this article to other individuals for non-commercial use, provided that the text, html codes, and this notice remain intact and unaltered in any way. Our Immune System may not be resold, reprinted or redistributed for compensation of any kind without prior written permission from Immune Deficiency Foundation. If you have any questions about permission, please contact: Immune Deficiency Foundation, 40 West Chesapeake Avenue, Suite 308, Towson, MD 21204, USA; or by telephone at 1-800-296-4433. -
Guidelines for Writing Examination Items (Questions)
Guidelines for Writing Examination Items (Questions) Enclosed are the content outlines for the Immunology certification examinations. The content outline specifies the breakdown of content and overall structure of the examination and indicates how many test questions are assigned to each topic area from a total of 70 questions. The content outline will guide you in creating new items to match certain topic areas. We would appreciate at least two (2) new items for each major roman numeral on the content outline(s). This means we are asking you to write two items for Roman numeral I, two items for Roman numeral II, and so on for each of the Roman numeral sections of the Content Outline. We would appreciate items submitted in advance, preferably no later than Tuesday, February 25, 2020. • Please use the “Item Writing Template” to create your new items. This is the proper format to be used for all items you submit. Font: Times New Roma. Font Size: 11 • Please identify the Content Outline position for each item (e.g., Chemistry Content Outline, Roman numeral I. “Proteins”, A. “Total Proteins” should be noted as “I.A.”). • New items must be multiple choice with four (4) possible answers. Remember to avoid "double negatives," "not" questions (e.g., "Which of the following is NOT true?"), and those allowing "all (or none) of the above," or "a and b" as a possible answer. • Each new item that you create must be accompanied with a reference [Author, Publication Year, Title, Edition, Page Number(s)] containing the correct answer. IMPORTANT: references must be from an AAB Review Manual, Governmental Regulations, Association or World Health Organization (WHO) Guidelines, or a text or manual published within the last six (6) years. -
Eosinophil Cytolysis and Release of Cell-Free Granules
CORRESPONDENCE LINK TO ORIGINAL ARTICLE LINK TO INITIAL CORRESPONDENCE to determine what conditions in vivo favour piecemeal degranulation and what condi- Eosinophil cytolysis and release of tions promote cytolysis (with or without ‘net’ formation) and release of intact granules. cell-free granules There are several strong recent reviews cover- ing mechanisms of degranulation, including 10 Helene F. Rosenberg and Paul S. Foster those written by Neves and Weller , and Lacy and Moqbel11, for those seeking greater insight into this important and evolving field. We are grateful for an excellent oppor- The results of eosinophil cytolysis — Helene F. Rosenberg is in the Inflammation tunity to expand on our recent Review specifically, the release of intact granules — Immunobiology Section, National Institute of Allergy (Eosinophils: changing perspectives in are not new findings. There have been many and Infectious Diseases, National Institutes of Health, health and disease. Nature Rev. Immunol. reports of free granules in tissues found in Bethesda, Maryland 20892, USA. 13, 9–22 (2013))1 that has been provided by conjunction with eosinophil-associated dis- Paul S. Foster is at the Priority Research Center the correspondence from Carl Persson and eases, including allergic rhinitis, bronchial for Asthma and Respiratory Diseases, Hunter Medical Research Institute and School of Lena Uller (Primary lysis of eosinophils asthma, atopic dermatitis, urticaria and Biomedical Sciences and Pharmacy, Faculty of Health, 7 as a major mode of activation of eosino- eosinophilic esophagitis . However, it was University of Newcastle, Newcastle, New South Wales, phils in human diseased tissues. Nature not clear what role these granules had, if any, 2300, Australia. -
Theory of an Immune System Retrovirus
Proc. Nati. Acad. Sci. USA Vol. 83, pp. 9159-9163, December 1986 Medical Sciences Theory of an immune system retrovirus (human immunodeficiency virus/acquired immune deficiency syndrome) LEON N COOPER Physics Department and Center for Neural Science, Brown University, Providence, RI 02912 Contributed by Leon N Cooper, July 23, 1986 ABSTRACT Human immunodeficiency virus (HIV; for- initiates clonal expansion, sustained by interleukin 2 and y merly known as human T-cell lymphotropic virus type interferon. Ill/lymphadenopathy-associated virus, HTLV-Ill/LAV), the I first give a brief sketch of these events in a linked- retrovirus that infects T4-positive (helper) T cells of the interaction model in which it is assumed that antigen-specific immune system, has been implicated as the agent responsible T cells must interact with the B-cell-processed virus to for the acquired immune deficiency syndrome. In this paper, initiate clonal expansion (2). I then assume that virus-specific I contrast the growth of a "normal" virus with what I call an antibody is the major component ofimmune system response immune system retrovirus: a retrovirus that attacks the T4- that limits virus spread. As will be seen, the details of these positive T cells of the immune system. I show that remarkable assumptions do not affect the qualitative features of my interactions with other infections as well as strong virus conclusions. concentration dependence are general properties of immune Linked-Interaction Model for Clonal Expansion of Lympho- system retroviruses. Some of the consequences of these ideas cytes. Let X be the concentration of normal infecting virus are compared with observations. -
Allergen-Specific Igg1 and Igg3 Through Fc Gamma RII Induce Eosinophil Degranulation
Allergen-specific IgG1 and IgG3 through Fc gamma RII induce eosinophil degranulation. M Kaneko, … , G J Gleich, H Kita J Clin Invest. 1995;95(6):2813-2821. https://doi.org/10.1172/JCI117986. Research Article Evidence suggests that eosinophils contribute to inflammation in bronchial asthma by releasing chemical mediators and cytotoxic granule proteins. To investigate the mechanism of eosinophil degranulation in asthma, we established an in vitro model of allergen-induced degranulation. We treated tissue culture plates with short ragweed pollen (SRW) extract and sera from either normal donors or SRW-sensitive patients with asthma. Eosinophils were incubated in the wells and degranulation was assessed by measurement of eosinophil-derived neurotoxin in supernatants. We detected degranulation only when sera from SRW-sensitive patients were reacted with SRW. Anti-IgG and anti-Fc gamma RII mAb, but not anti-IgE or anti-Fc epsilon RII mAb, abolished the degranulation. IgG-depleted serum did not induce degranulation; IgE-depleted serum triggered as much degranulation as untreated serum. Furthermore, serum levels of SRW-specific IgG1 or IgG3 correlated with the amounts of released eosinophil-derived neurotoxin. When eosinophils were cultured in wells coated with purified IgG or IgE, eosinophil degranulation was observed only with IgG. Finally, human IgG1 and IgG3, and less consistently IgG2, but not IgG4, induced degranulation. Thus, sera from patients with SRW-sensitive asthma induce eosinophil degranulation in vitro through antigen-specific IgG1 and IgG3 antibodies. These antibodies may be responsible for degranulation of eosinophils in inflammatory reactions, such as bronchial asthma. Find the latest version: https://jci.me/117986/pdf Allergen-specific IgG1 and IgG3 through FcRIl Induce Eosinophil Degranulation Masayuki Kaneko, Mark C. -
El Paso Community College Syllabus Part II Official Course Description
MLAB 1235; Revised Fall 2019/Spring 2020 El Paso Community College Syllabus Part II Official Course Description SUBJECT AREA Medical Laboratory Technology COURSE RUBRIC AND NUMBER MLAB 1235 COURSE TITLE Immunology/Serology COURSE CREDIT HOURS 2 1 : 3 Credits Lec Lab I. Catalog Description Provides an introduction to the theory and application of basic immunology, including the immune response, principles of antigen-antibody reactions, and the principles of serological procedures as well as quality control, quality assurance, and lab safety. A grade of “C” or better is required in this course to take the next course. Corequisite: MLAB 1260. (1:3). Lab fee. II. Course Objectives A. Unit I. Laboratory Operations Upon satisfactory completion of this unit, the student will be able to: 1. Demonstrate adherence to Standard Precautions and the organizations’ SOP (Standard Operating Procedures) at all times. 2. Discuss legal and ethical concerns pertaining to Patient Informed Consent, Standard of Care, and HIPAA regulations. 3. Compliance with government, state, and organizational safety regulations involving Biological, Chemical, Radioactive, Fire, Physical, and Electrical hazards. 4. Explain the importance of actively participating in Quality Assurance, Quality Control and Proficiency Testing protocols incorporating precision, accuracy, Levi Jennings Charts and Westgard Rules. 5. Locate and make use of MSDS (Material Safety Data Sheets) 6. Discuss how OSHA affects safety, health, and compliance policies in the workplace. 7. Discuss nosocomial infections and identify the basic programs for infection control. 8. Identify the potential routes of infection and methods for preventing transmission of microorganisms through these routes. 9. Explain the proper techniques for hand washing, gowning, gloving, and masking. -
Practice Parameter for the Diagnosis and Management of Primary Immunodeficiency
Practice parameter Practice parameter for the diagnosis and management of primary immunodeficiency Francisco A. Bonilla, MD, PhD, David A. Khan, MD, Zuhair K. Ballas, MD, Javier Chinen, MD, PhD, Michael M. Frank, MD, Joyce T. Hsu, MD, Michael Keller, MD, Lisa J. Kobrynski, MD, Hirsh D. Komarow, MD, Bruce Mazer, MD, Robert P. Nelson, Jr, MD, Jordan S. Orange, MD, PhD, John M. Routes, MD, William T. Shearer, MD, PhD, Ricardo U. Sorensen, MD, James W. Verbsky, MD, PhD, David I. Bernstein, MD, Joann Blessing-Moore, MD, David Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD, Christopher R. Randolph, MD, Diane Schuller, MD, Sheldon L. Spector, MD, Stephen Tilles, MD, Dana Wallace, MD Chief Editor: Francisco A. Bonilla, MD, PhD Co-Editor: David A. Khan, MD Members of the Joint Task Force on Practice Parameters: David I. Bernstein, MD, Joann Blessing-Moore, MD, David Khan, MD, David Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD, Christopher R. Randolph, MD, Diane Schuller, MD, Sheldon L. Spector, MD, Stephen Tilles, MD, Dana Wallace, MD Primary Immunodeficiency Workgroup: Chairman: Francisco A. Bonilla, MD, PhD Members: Zuhair K. Ballas, MD, Javier Chinen, MD, PhD, Michael M. Frank, MD, Joyce T. Hsu, MD, Michael Keller, MD, Lisa J. Kobrynski, MD, Hirsh D. Komarow, MD, Bruce Mazer, MD, Robert P. Nelson, Jr, MD, Jordan S. Orange, MD, PhD, John M. Routes, MD, William T. Shearer, MD, PhD, Ricardo U. Sorensen, MD, James W. Verbsky, MD, PhD GlaxoSmithKline, Merck, and Aerocrine; has received payment for lectures from Genentech/ These parameters were developed by the Joint Task Force on Practice Parameters, representing Novartis, GlaxoSmithKline, and Merck; and has received research support from Genentech/ the American Academy of Allergy, Asthma & Immunology; the American College of Novartis and Merck. -
A Challenging Case of Igd Kappa Multiple Myeloma Associated with Primary Amyloidosis: Importance of Serum Free Light Chains in M
L al of euk rn em u i o a J Journal of Leukemia García de Veas Silva JL et al, J Leuk 2014, 2:5 ISSN: 2329-6917 DOI: 10.4172/2329-6917.1000164 Case Report Open Access A Challenging Case of IgD Kappa Multiple Myeloma Associated With Primary Amyloidosis: Importance of Serum Free Light Chains in Monitoring Treatment Response and Disease Relapse José Luis García de Veas Silva1*, Carmen Bermudo Guitarte1, Paloma Menéndez Valladares1, Rafael Duro Millán2 and Johanna Carolina Rojas Noboa2 1Department of Clinical Biochemistry, Hospital Universitario Virgen Macarena, Sevilla, Spain 2Department of Hematology, Hospital Universitario Virgen Macarena, Sevilla, Spain *Corresponding author: José Luis García de Veas Silva, Laboratory of Proteins, Department of Clinical Biochemistry, Hospital Universitario Virgen Macarena, Sevilla, Spain, Tel: +034955008108; E-mail: [email protected] Rec date: Oct 10, 2014, Acc date: Oct 16, 2014; Pub date: Oct 24, 2014 Copyright: © 2014 García de Veas Silva JL, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Multiple Myeloma (MM) is a malignancy of B cells characterized by an atypical proliferation of plasma cells. IgD MM has a very low incidence (2% of total MM cases) and it´s characterized by an aggressive course and a worse prognosis than other subtypes. The serum free light chains (sFLC) are very important markers for monitoring patients with MM and other monoclonal gammopathies. When the sFLC are present in low concentrations, it is often difficult to detect them by conventional methods such as serum protein electrophoresis and serum immunofixation. -
Differential Release of Mast Cell Mediators and the Pathogenesis Of
Theoharis C. Theoharides Differential release of mast cell Duraisamy Kempuraj Michael Tagen mediators and the pathogenesis of Pio Conti inflammation Dimitris Kalogeromitros Authors’ addresses Summary: Mast cells are well known for their involvement in allergic and Theoharis C. Theoharides1,2,3,4, Duraisamy Kempuraj1, Michael Tagen1, anaphylactic reactions, during which immunoglobulin E (IgE) receptor Pio Conti5, Dimitris Kalogeromitros4 (FceRI) aggregation leads to exocytosis of the content of secretory granules 1Laboratory of Molecular Immunopharmacology and Drug (1000 nm), commonly known as degranulation, and secretion of multiple Discovery, Department of Pharmacology and Experimental mediators. Recent findings implicate mast cells also in inflammatory Therapeutics, Tufts University School of Medicine diseases, such as multiple sclerosis, where mast cells appear to be intact by and Tufts – New England Medical Center, Boston, MA, USA. light microscopy. Mast cells can be activated by bacterial or viral antigens, 2Department of Biochemistry, Tufts University School of cytokines, growth factors, and hormones, leading to differential release of Medicine and Tufts – New England Medical Center, Boston, distinct mediators without degranulation. This process appears to involve MA, USA. de novo synthesis of mediators, such as interleukin-6 and vascular endothelial 3Department of Internal Medicine, Tufts University School growth factor, with release through secretory vesicles (50 nm), similar to of Medicine and Tufts – New England Medical Center, those in synaptic transmission. Moreover, the signal transduction steps Boston, MA, USA. necessary for this process appear to be largely distinct from those known in 4Allergy Section, Attikon Hospital, Athens, Medical School, FceRI-dependent degranulation. How these differential mast cell responses Athens, Greece. are controlled is still unresolved. -
Human Antibody-Dependent Cellular Cytotoxicity-Mediating Antibodies Do Not Recruit Non-Human Primate CD20+ NK Cells Stephanie Asdell, R
Human Antibody-Dependent Cellular Cytotoxicity-Mediating Antibodies Do Not Recruit Non-Human Primate CD20+ NK Cells Stephanie Asdell, R. Whitney Edwards, Shalini Jha, Dr. Guido Ferrari Department of Surgery and Molecular Genetics and Microbiology Introduction Results Results • The antibody-dependent cell-mediated cytotoxicity 1) How does the % NK in the effector population 4) Do CD20+ NK populations play a role in the ADCC (ADCC) response represents one of mechanisms affect ADCC activity? response? Figure 3: We through which the immune system destroys HIV-1 NK Purity measured levels of infected cells. CD107a in 4 NHP • ADCC responses in non primate (NHP) models, PBMC and 5 which are used to study protection from HIV-1 in splenocyte samples. preclinical trials to translate for human use, have not The threshold of been well characterized to date. positivity was 0.396%. Results: Using • In ADCC, natural killer (NK) cells are recruited by C11_WT human Ab natural infection- or vaccine-induced antibodies (Abs) and JR4 NHP Ab, the bound to the HIV-1 envelope glycoproteins expressed difference in the on infected CD4+ T-cells via Fc-γ Receptor IIIA . Figure 1: Population of NK was determined from live lymph cells proportion of CD8- that are CD3-, CD20-, CD16+. The x-axes represent one or more • NK cells’ recognition of the infected cells leads to the NKG2a- CD107A+ human (left figure) or NHP (right two figures) donors, and the y- cells was not release granzymes and perforin by degranulation, axes represent the % of live lymph cells that are NK. statistically significant triggering apoptotic signal pathways in the infected Results: In previous experiments, we showed that the NHP between CD20- and cells and ultimately causing their elimination. -
Acquired Immunodeficiency Syndrome (Aids)
ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) What is Acquired Immunodeficiency Syndrome (AIDS)? AIDS stands for Acquired Immunodeficiency Syndrome. The term AIDS refers to an advanced stage of HIV infection. People are said to have AIDS when they have certain signs or symptoms specified in guidelines formulated by the U.S. Centers for Disease Control and Prevention (CDC). What causes AIDS? AIDS is caused by HIV (human immunodeficiency virus). By killing or damaging cells of the body's immune system, HIV progressively destroys the body's ability to fight infections and certain cancers. What are the signs and symptoms of AIDS? Symptoms of opportunistic infections common in people with AIDS include: • Coughing and shortness of breath • Seizures and lack of coordination • Difficult or painful swallowing • Mental symptoms such as confusion and forgetfulness • Severe and persistent diarrhea • Fever • Vision loss • Nausea, abdominal cramps, and vomiting • Weight loss and extreme fatigue • Severe headaches • Coma How is AIDS diagnosed? A diagnosis of AIDS is made by a physician using laboratory test results and clinical criteria such as AIDS indicator illnesses. Contact Number: STD Program, (302)-744-1050 Revised: 08/2013 Page 1 of 2 How is AIDS treated? Drugs approved for the treatment of HIV/AIDS fall into four classes, which are: 1. Nucleoside or nucleotide reverse transcriptase inhibitors. NRTIs work by blocking the enzyme reverse transcriptase, which helps the virus make DNA from its RNA. 2. Non-nucleoside reverse transcriptase inhibitors. NNRTIs work like the ones listed above. 3. Protease inhibitors. PIs work completely differently from those listed above. HIV produces an enzyme called protease (pronounced PRO-tee-ace) in the late stages of its reproduction.