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Table of Contents
Vol. 118, No. 2-4, 1999
Issue release date: February – April
Section title: Biology of Inflammatory Products: Cytokines
Int Arch Allergy Immunol 1999;118:108–111
(DOI:10.1159/000024042)

TNF–· and IL–5 Gene Induction in IgE plus Antigen–Stimulated Mast Cells Require Common and Distinct Signaling Pathways

Baumruker T. · Csonga R. · Jaksche D. · Novotny V. · Prieschl E.E.
Department of Immunology, Novartis Research Institute, Vienna, Austria

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Article / Publication Details

First-Page Preview
Abstract of Biology of Inflammatory Products: Cytokines

Published online: April 23, 1999
Issue release date: February – April

Number of Print Pages: 4
Number of Figures: 2
Number of Tables: 0

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

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

Abstract

Background: Mast cells produce a variety of cytokines and chemokines in a timely and tightly controlled fashion if stimulated via the FcεRI. Evidence is accumulating that the transcriptional induction of the corresponding genes and the release of these mediators are dependent on common and mediator–specific components of the signal transduction and transcription factor machinery. Methods: We addressed this issue by comparing the effects of mitogen activated protein (MAP) kinase pathway inhibitors and protein kinase C (PKC) inhibitors on the induction of TNF–α and IL–5 after IgE plus antigen (Ag) stimulation in CPII mouse mast cells using Western blot analyses and transient transfections of reporter gene plasmids. Results: TNF–α shows a strict dependence on the MAP kinase pathway, while IL–5 is either activated by PMA–dependent PKCs or along the MAP kinase pathway. In addition, both mediators are sensitive to PKCμ inhibition, suggesting involvement of this atypical, non–PMA dependent PKC in the overall induction process. Conclusion: While the two cytokines were recently shown to be regulated by a member of the nuclear factor of activated T–cells (NF–AT) transcription factor family, activator protein 1 (AP1) was identified as a cofactor at the TNF–α promoter while a GATA family member comprised the cofactor at the IL–5 promoter. This suggests that the differences in requirement for signal transduction cascades are the result of a different usage of NF–AT cofactors for transcription of each cytokine in mast cells.


Article / Publication Details

First-Page Preview
Abstract of Biology of Inflammatory Products: Cytokines

Published online: April 23, 1999
Issue release date: February – April

Number of Print Pages: 4
Number of Figures: 2
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.