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Table of Contents
Vol. 144, No. 4, 2007
Issue release date: November 2007
Section title: Original Paper
Int Arch Allergy Immunol 2007;144:305–314
(DOI:10.1159/000106319)

Differential Role of Thymic Stromal Lymphopoietin in the Induction of Airway Hyperreactivity and Th2 Immune Response in Antigen-Induced Asthma with Respect to Natural Killer T Cell Function

Nagata Y.a · Kamijuku H.b · Taniguchi M.a · Ziegler S.c · Seino K.a, b
aLaboratory for Immune Regulation, RIKEN Research Center for Allergy and Immunology, Yokohama, and bLaboratory for Molecular Therapy, Institute of Medical Science, St. Marianna University, Kawasaki, Japan; cBenaroya Research Institute at Virginia Mason and Department of Immunology, University of Washington, Seattle, Wash., USA

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: November 21, 2006
Accepted: April 11, 2007
Published online: July 23, 2007
Issue release date: November 2007

Number of Print Pages: 10
Number of Figures: 8
Number of Tables: 0

ISSN: 1018-2438 (Print)
eISSN: 1423-0097 (Online)

For additional information: http://www.karger.com/IAA

Abstract

Asthma is an inflammatory lung disease, in which CD1d-restricted natural killer T (NKT) cells play an importantpathogenic role. Also, recent reports indicated that a cytokine, thymic stromal lymphopoietin (TSLP), is essential for the development of antigen-induced asthma. Here we examined the relationship between NKT cells and TSLP in a mouse model of asthma. NKT cells express TSLP receptor as well as IL-7 receptor α-chain. TSLP acts on NKT cells to preferentially increase their IL-13 production but not IFN-γ and IL-4. In an allergen-induced asthma model, the development of airway hyperreactivity, a cardinal feature of asthma, was increased in TSLP transgenic mice, whereas this effect was not observed in TSLP transgenic mice lacking NKT cells. Interestingly, in the NKT cell-lacking TSLP transgenic mice, pulmonary eosinophilia and increase in IgE did not improve. Pulmonary lymphocytes from the NKT cell-lacking TSLP transgenic mice produced much less IL-13 upon CD3 stimulation than those from NKT cell-competent TSLP transgenic mice. These resultssuggest that, in allergen-induced asthma, TSLP acts on NKT cells to enhance airway hyperreactivity by upregulating their IL-13 production, whereas eosinophilia and IgE production are not influenced.

© 2007 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: November 21, 2006
Accepted: April 11, 2007
Published online: July 23, 2007
Issue release date: November 2007

Number of Print Pages: 10
Number of Figures: 8
Number of Tables: 0

ISSN: 1018-2438 (Print)
eISSN: 1423-0097 (Online)

For additional information: http://www.karger.com/IAA


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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 government 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.