The Journal of Experimental Medicine
Avanti Polar Lipids, Inc.
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online 6 August 2001. doi:10.1084/jem.194.3.355
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 232K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Helmby, H.
Right arrow Articles by Grencis, R. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Helmby, H.
Right arrow Articles by Grencis, R. K.
Right arrowPubmed/NCBI databases
*Substance via MeSH
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?
© The Rockefeller University Press, 0022-1007/2001/8/355/ $5.00
The Journal of Experimental Medicine, Volume 194, Number 3, August 6, 2001 355-364

Original Article

Interleukin (Il)-18 Promotes the Development of Chronic Gastrointestinal Helminth Infection by Downregulating IL-13

Helena Helmbya, Kiyoshi Takedab, Shizuo Akirab, and Richard K. Grencisa

a School of Biological Sciences, The University of Manchester, Manchester M13 9PT, UK
b Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan
School of Biological Sciences, Stopford Building 3.239, The University of Manchester, Manchester M13 9PT, UK.44-161-275-564044-161-275-5319

helena.e.helmby{at}man.ac.uk

Expulsion of the gastrointestinal nematode Trichuris muris is mediated by a T helper (Th) 2 type response involving interleukin (IL)-4 and IL-13. Here we show that Th1 response–associated susceptibility involves prior activation of IL-18 and caspase-1 followed by IL-12 and interferon (IFN)-{gamma} in the intestine. IL-18–deficient mice are highly resistant to chronic T. muris infection and in vivo treatment of normal mice with recombinant (r)IL-18 suppresses IL-13 and IL-4 secretion but does not affect IFN-{gamma}.

In vivo treatment of T. muris–infected IFN-{gamma}–deficient mice with rIL-18 demonstrated that the inhibitory effect of IL-18 on IL-13 secretion is independent of IFN-{gamma}. Hence, IL-18 does not function as an IFN-{gamma}–inducing cytokine during chronic T. muris infection but rather as a direct regulator of Th2 cytokines. These results provide the first demonstration of the critical role of IL-18 in regulating Th cell responses during gastrointestinal nematode infection.

Key Words: Th cell • cytokine • mucosa • nematode • regulation

Abbreviations used in this paper: ES, excretory/secretory; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; KO, knockout; MLN, mes-enteric lymph node; p.i., post infection; r, recombinant; RPA, RNase protection assay; WT, wild-type.

© 2001 The Rockefeller University Press


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS