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B Cell Trophic Factors and B Cell Antagonism in Autoimmune Disease

Editor(s): Stohl W. (Los Angeles, Calif.) 
Table of Contents
Vol. 8, No. , 2005
Section title: Paper
Stohl W (ed): B Cell Trophic Factors and B Cell Antagonism in Autoimmune Disease. Curr Dir Autoimmun. Basel, Karger, 2005, vol 8, pp 55-90
(DOI:10.1159/000082087)

The CD19-CD21 Signal Transduction Complex of B Lymphocytes Regulates the Balance between Health and Autoimmune Disease: Systemic Sclerosis as a Model System

Tedder T.F. · Poe J.C. · Fujimoto M. · Haas K.M. · Sato S.
aDepartment of Immunology, Duke University Medical Center, Durham, N.C., USA; bDepartment of Dermatology, Faculty of Medicine, University of Tokyo, Bunkyo, Tokyo, and cDepartment of Dermatology, Kanazawa University Graduate School of Medical Science, Ishikawa, Kanazawa, Japan

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 12/10/2004
Cover Date: 2005

Number of Print Pages: 36
Number of Figures: 0
Number of Tables: 0

ISBN: 978-3-8055-7851-6 (Print)
eISBN: 978-3-318-01165-4 (Online)

Abstract

Cell-surface CD19 functions as a general rheostat for defining intrinsic and antigen receptor-induced signaling thresholds critical for clonal expansion of the B cell pool and humoral immunity. CD19 also governs B cell responses initiated through the CD21 receptor, where complement C3d binding to CD21 links humoral immune responses with the innate immune system. Alterations in this signaling pathway can predispose mice and humans to autoantibody production and systemic autoimmunity. Transgenic mice that overexpress CD19 by 20-170% lose tolerance and generate autoantibodies. Likewise, B cells from CD21-deficient mice overexpress CD19 by ~ 50%, which leads to autoantibody production. Autoimmune patients with systemic sclerosis also overexpress CD19 by ~20%, which may contribute to their intrinsic B cell abnormalities and autoantibody production. Thus, chronic B cell activation resulting from augmented CD19 expression or signaling through the CD19 pathway may reveal a prototype autoimmune disease susceptibility pathway in mice and humans.


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 12/10/2004
Cover Date: 2005

Number of Print Pages: 36
Number of Figures: 0
Number of Tables: 0

ISBN: 978-3-8055-7851-6 (Print)
eISBN: 978-3-318-01165-4 (Online)


Copyright / Drug Dosage

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.