Allergen-Specific Igg1 and Igg3 Through Fc Gamma RII Induce Eosinophil Degranulation
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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. -
Eosinophils but Not of Neutrophils Stimulates Effector Functions of Human Interaction with Secretory Component
Interaction with Secretory Component Stimulates Effector Functions of Human Eosinophils But Not of Neutrophils This information is current as Youichi Motegi and Hirohito Kita of September 23, 2021. J Immunol 1998; 161:4340-4346; ; http://www.jimmunol.org/content/161/8/4340 Downloaded from References This article cites 49 articles, 20 of which you can access for free at: http://www.jimmunol.org/content/161/8/4340.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 23, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 1998 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Interaction with Secretory Component Stimulates Effector Functions of Human Eosinophils But Not of Neutrophils1 Youichi Motegi and Hirohito Kita2 Eosinophils and their products are important in the pathophysiology of allergic inflammation in mucosal tissues. Secretory component bound to IgA mediates transepithelial transport of IgA and confers increased stability on the resultant secretory IgA; however, the effect of secretory component on the biologic activity of IgA is unknown. -
Detailed Structure and Pathophysiological Roles of the Iga-Albumin Complex in Multiple Myeloma
International Journal of Molecular Sciences Article Detailed Structure and Pathophysiological Roles of the IgA-Albumin Complex in Multiple Myeloma Yuki Kawata 1, Hisashi Hirano 1, Ren Takahashi 1, Yukari Miyano 1, Ayuko Kimura 1, Natsumi Sato 1, Yukio Morita 2, Hirokazu Kimura 1,* and Kiyotaka Fujita 1 1 Department of Health Sciences, Gunma Paz University Graduate School of Health Sciences, 1-7-1, Tonyamachi, Takasaki-shi, Gunma 370-0006, Japan; [email protected] (Y.K.); [email protected] (H.H.); [email protected] (R.T.); [email protected] (Y.M.); [email protected] (A.K.); [email protected] (N.S.); [email protected] (K.F.) 2 Laboratory of Public Health II, Azabu University School of Veterinary Medicine, 1-17-71, Fuchinobe, Chuo-ku, Sagamihara, Kanagawa 252-5201, Japan; [email protected] * Correspondence: [email protected]; Tel.: +81-27-365-3366; Fax: +81-27-388-0386 Abstract: Immunoglobulin A (IgA)-albumin complexes may be associated with pathophysiology of multiple myeloma, although the etiology is not clear. Detailed structural analyses of these protein– protein complexes may contribute to our understanding of the pathophysiology of this disease. We analyzed the structure of the IgA-albumin complex using various electrophoresis, mass spectrom- etry, and in silico techniques. The data based on the electrophoresis and mass spectrometry showed that IgA in the sera of patients was dimeric, linked via the J chain. Only dimeric IgA can bind to albumin molecules leading to IgA-albumin complexes, although both monomeric and dimeric forms of IgA were present in the sera. -
Different Innate and Adaptive Immune Response to SARS-Cov-2 Infection of Asymptomatic, Mild and Severe Cases
medRxiv preprint doi: https://doi.org/10.1101/2020.06.22.20137141; this version posted September 28, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license . Title: Different innate and adaptive immune response to SARS-CoV-2 infection of asymptomatic, mild and severe cases Rita Carsetti1,2*, Salvatore Zaffina3,4, Eva Piano Mortari1#, Sara Terreri1#, Francesco Corrente2, Claudia Capponi2, Patrizia Palomba2, Mattia Mirabella2, Simona Cascioli5, Paolo Palange6, Ilaria Cuccaro6, Cinzia Milito7, Alimuddin Zumla8,9, Markus Maeurer10,11, Vincenzo Camisa3,4, Maria Rosaria Vinci3,4, Annapaola Santoro3,4, Eleonora Cimini12, Luisa Marchioni13, Emanuele Nicastri13, Fabrizio Palmieri13, Chiara Agrati12, Giuseppe Ippolito14, Ottavia Porzio15,16, Carlo Concato17, Andrea Onetti Muda18, Massimiliano Raponi4, Concetta Quintarelli19,20, Isabella Quinti7, Franco Locatelli19,21 Affiliations: 1B Cell Pathophysiology Unit, Immunology Research Area, Bambino Gesù Children's Hospital IRCCS, Rome, Italy; 2Diagnostic Immunology Unit, Department of Laboratories, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy 3Occupational Medicine/Health Technology Assessment and Safety Research Unit, Clinical- Technological Innovations Research Area, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy 4Health Directorate, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy 5Research Laboratories, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy 6Department of Public Health and infectious diseases pulmonary division, Policlinico Umberto I Hospital, Rome, Italy. 7Department of Molecular Medicine, Sapienza University of Rome, Rome, Italy NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. -
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. -
The Effect of Mirthful Laughter on Stress and Natural Killer Cell Activity
Western Kentucky University TopSCHOLAR® Nursing Faculty Publications School of Nursing 2003 The ffecE t of Mirthful Laughter on Stress and Natural Killer Cell Activity Mary P. Bennett Western Kentucky University, [email protected] Janice M. Zeller Lisa Rosenberg Judith McCann Follow this and additional works at: http://digitalcommons.wku.edu/nurs_fac_pub Part of the Alternative and Complementary Medicine Commons, Nursing Commons, and the Oncology Commons Recommended Repository Citation Bennett, Mary P.; Zeller, Janice M.; Rosenberg, Lisa; and McCann, Judith. (2003). The Effect of Mirthful Laughter on Stress and Natural Killer Cell Activity. Alternative Therapies in Health and Medicine, 9 (2), 38-45. Available at: http://digitalcommons.wku.edu/nurs_fac_pub/9 This Other is brought to you for free and open access by TopSCHOLAR®. It has been accepted for inclusion in Nursing Faculty Publications by an authorized administrator of TopSCHOLAR®. For more information, please contact [email protected]. original research THE EFFECT OF MIRTHFUL LAUGHTER ON STRESS AND NATURAL KILLER CELL ACTIVITY Mary P. Bennett, DNSc, RN, Janice M. Zeller, PhD, RN, FAAN, Lisa Rosenberg, PhD, RN, Judith McCann, DNSc, RN Mary P. Bennett is associate professor and assistant dean, function postintervention (t16 =2.52 P=.037) and compared with the Indiana State University School of Nursing in Terre Haute, Ind. remaining participants (t32=32.1; P=.04). Humor response scale scores Janice M. Zeller is professor, Department of Adult Health correlated with changes in NK cell activity (r16=.744;P =.001). Nursing and associate professor, Department of Conclusion • Laughter may reduce stress and improve NK cell activity. As Immunology/Microbiology; and Lisa Rosenberg is assistant pro- low NK cell activity is linked to decreased disease resistance and increased fessor, Department of Community and Mental Health Nursing morbidity in persons with cancer and HIV disease, laughter may be a useful and associate dean, Student Affairs, College of Nursing, at Rush cognitive-behavioral intervention. -
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. -
IG Living Magazine April-May 2018
April-May 2018 IGLiving.com Staying Active How to Keep Moving with Chronic Illness Planning Travel? Follow These Simple Steps Exercises for Better Balance What Is Now Known Assistive Devices About SAD? for Staying Mobile On IGLiving.com Feaatures an easy- to-nnavigate design Indepth content onn IG-treated diseases annd treatment Cononnnnectnne withh oouurur Pattiiieeent Advocateee,, AAbbbbie Cornett RReeaead weeklyklylyy bblogs about isssues relal tted d to living with cchchrhroononionic illnessnessessessss Valuablee Resourcees and more On Facebook Findd timely and relevant informao tion posted dailyy, providing a venue foro connnecting with others in the IG community. On the Go CONTENTS | April-May 2018 Features Up Front 16 Travel Tips for Those 5 Editorial with Chronic Illness Staying Active with By Abbie Cornett and Chronic Illness Ronale Tucker Rhodes, MS By Ronale Tucker Rhodes, MS 6 Abbie’s Corner 20 Exercises to Preventing Isolation Improve Balance By Abbie Cornett By Matthew D. Hansen, DPT, MPT, BSPTS 7 Faces of IG From our Facebook page 24 Specific Antibody Deficiency and/or Impaired Polysaccharide Responsiveness Departments By E. Richard Stiehm, MD 8 Ask the Experts 32 Understanding Healthcare professionals’ NK Cell Deficiency responses to patient questions By Jordan S. Orange, MD, PhD 9 Immunology 101 DiGeorge Syndrome: Thymus Development and the Initiation of T Lymphocyte Development Sources By Terry O. Harville, MD, PhD 42 Product Guide 10 Clinical Brief Mobility Management What Are Immunoglobulins? By Trudie Mitschang By Michelle Greer, RN 44 Book Corner 12 In the News New and useful reading Research, science, product and insurance updates 46 Resource Center Community foundations, associations, forums and other resources Columns 36 Let’s Talk!—SamMichael Long Advertising in IG Living By Trudie Mitschang IG Living Magazine is read by 30,000 subscribers who are patients that depend upon immune globulin products and their healthcare providers. -
Major Histocompatibility Complex Class III Genes and Susceptibility to Immunoglobulin a Deficiency and Common Variable Immunodeficiency
Major histocompatibility complex class III genes and susceptibility to immunoglobulin A deficiency and common variable immunodeficiency. J E Volanakis, … , H W Schroeder Jr, M D Cooper J Clin Invest. 1992;89(6):1914-1922. https://doi.org/10.1172/JCI115797. Research Article We have proposed that significant subsets of individuals with IgA deficiency (IgA-D) and common variable immunodeficiency (CVID) may represent polar ends of a clinical spectrum reflecting a single underlying genetic defect. This proposal was supported by our finding that individuals with these immunodeficiencies have in common a high incidence of C4A gene deletions and C2 rare gene alleles. Here we present our analysis of the MHC haplotypes of 12 IgA-D and 19 CVID individuals from 21 families and of 79 of their immediate relatives. MHC haplotypes were defined by analyzing polymorphic markers for 11 genes or their products between the HLA-DQB1 and the HLA-A genes. Five of the families investigated contained more than one immunodeficient individual and all of these included both IgA-D and CVID members. Analysis of the data indicated that a small number of MHC haplotypes were shared by the majority of immunodeficient individuals. At least one of two of these haplotypes was present in 24 of the 31 (77%) immunodeficient individuals. No differences in the distribution of these haplotypes were observed between IgA-D and CVID individuals. Detailed analysis of these haplotypes suggests that a susceptibility gene or genes for both immunodeficiencies are located within the class III region of the MHC, possibly between the C4B and C2 genes. Find the latest version: https://jci.me/115797/pdf Major Histocompatibility Complex Class Ill Genes and Susceptibility to Immunoglobulin A Deficiency and Common Variable Immunodeficiency John E. -
Immunology: Antibody Basics 2
John A. Burns School of Medicine JABSOM e-Learning for Basic Sciences e-Learning To navigate: 1 1. Yellow navigation bar 2 Immunology: Antibody Basics 2. Back and Fwd buttons Estimated Learning Time: 30 min. 3 4 Back Fwd 5 One :: General Structure 6 7 Identify the Parts of an Antibody 8 Two :: Isotypes 9 Identify Antibody Isotypes 10 [ Start Now! ] 11 Three :: Function 12 Match Antibody Functions With Isotypes 13 14 Four :: Diversity 15 Explain Antibody Diversity 16 17 Antibody 18 Advice 19 20 21 Allow Hi! 22 me to be your Ctrl + L 23 Command + L guide... find me 24 FULL SCREEN at the bottom 25 in Adobe Acrobat of each page! 26 Contributors William L. Gosnell, Ph.D. Software Requirements: Kenton J. Kramer, Ph.D. Click to download Karen M. Yamaga, Ph.D. the latest versions Department of Tropical Medicine, Medical Microbiology and Pharmacology JABSOM John A. Burns School of Medicine e-Learning e-Learning for Basic Sciences OVERVIEW 1 2 3 Contents 4 5 instructional By the end of this module you should be This One :: General Structure 6 module was designed with you able to: Identify the Parts of an Antibody Page 3 7 in mind. Understanding antibody 1. Identify the parts of an antibody. basics will help you understand 2. Identify antibody isotypes. Two :: Isotypes 8 immunology concepts that are 3. Match antibody functions with isotypes. Identify Antibody Isotypes Page 9 9 necessary to pass USMLE board 4. Explain antibody diversity from 10 exams - the first step on your way somatic recombination. to becoming a doctor. -
Mouse and Human Fcr Effector Functions
Pierre Bruhns Mouse and human FcR effector € Friederike Jonsson functions Authors’ addresses Summary: Mouse and human FcRs have been a major focus of Pierre Bruhns1,2, Friederike J€onsson1,2 attention not only of the scientific community, through the cloning 1Unite des Anticorps en Therapie et Pathologie, and characterization of novel receptors, and of the medical commu- Departement d’Immunologie, Institut Pasteur, Paris, nity, through the identification of polymorphisms and linkage to France. disease but also of the pharmaceutical community, through the iden- 2INSERM, U760, Paris, France. tification of FcRs as targets for therapy or engineering of Fc domains for the generation of enhanced therapeutic antibodies. The Correspondence to: availability of knockout mouse lines for every single mouse FcR, of Pierre Bruhns multiple or cell-specific—‘a la carte’—FcR knockouts and the Unite des Anticorps en Therapie et Pathologie increasing generation of hFcR transgenics enable powerful in vivo Departement d’Immunologie approaches for the study of mouse and human FcR biology. Institut Pasteur This review will present the landscape of the current FcR family, 25 rue du Docteur Roux their effector functions and the in vivo models at hand to study 75015 Paris, France them. These in vivo models were recently instrumental in re-defining Tel.: +33145688629 the properties and effector functions of FcRs that had been over- e-mail: [email protected] looked or discarded from previous analyses. A particular focus will be made on the (mis)concepts on the role of high-affinity Acknowledgements IgG receptors in vivo and on results from antibody engineering We thank our colleagues for advice: Ulrich Blank & Renato to enhance or abrogate antibody effector functions mediated by Monteiro (FacultedeMedecine Site X. -
The Enigma of Eosinophil Degranulation
International Journal of Molecular Sciences Review The Enigma of Eosinophil Degranulation Timothée Fettrelet 1,2 , Lea Gigon 1, Alexander Karaulov 3 , Shida Yousefi 1 and Hans-Uwe Simon 1,3,4,5,* 1 Institute of Pharmacology, University of Bern, Inselspital, INO-F, CH-3010 Bern, Switzerland; [email protected] (T.F.); [email protected] (L.G.); shida.yousefi@pki.unibe.ch (S.Y.) 2 Department of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland 3 Department of Clinical Immunology and Allergology, Sechenov University, 119991 Moscow, Russia; [email protected] 4 Laboratory of Molecular Immunology, Institute of Fundamental Medicine and Biology, Kazan Federal University, 420012 Kazan, Russia 5 Institute of Biochemistry, Medical School Brandenburg, D-16816 Neuruppin, Germany * Correspondence: [email protected]; Tel.: +41-31-632-3281 Abstract: Eosinophils are specialized white blood cells, which are involved in the pathology of diverse allergic and nonallergic inflammatory diseases. Eosinophils are traditionally known as cytotoxic effector cells but have been suggested to additionally play a role in immunomodulation and maintenance of homeostasis. The exact role of these granule-containing leukocytes in health and diseases is still a matter of debate. Degranulation is one of the key effector functions of eosinophils in response to diverse stimuli. The different degranulation patterns occurring in eosinophils (piecemeal degranulation, exocytosis and cytolysis) have been extensively studied in the last few years. How- ever, the exact mechanism of the diverse degranulation types remains unknown and is still under investigation. In this review, we focus on recent findings and highlight the diversity of stimulation and methods used to evaluate eosinophil degranulation.