The Journal of Experimental Medicine
VeriKine-HS Human Interferon-Beta Serum
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 199K)
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 Zhong, G.
Right arrow Articles by Liu, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhong, G.
Right arrow Articles by Liu, L.
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, 0022-1007/1999/6/1931/ $5.00
The Journal of Experimental Medicine, Volume 189, Number 12, June 21, 1999 1931-1938

Articles

Chlamydia Inhibits Interferon {gamma}–inducible Major Histocompatibility Complex Class II Expression by Degradation of Upstream Stimulatory Factor 1

Guangming Zhong, Tao Fan, and Li Liu

From the Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba R3E OW3, Canada

We report that chlamydiae, which are obligate intracellular bacterial pathogens, can inhibit interferon (IFN)-{gamma}–inducible major histocompatibility complex (MHC) class II expression. However, the IFN-{gamma}–induced IFN regulatory factor-1 (IRF-1) and intercellular adhesion molecule 1 (ICAM-1) expression is not affected, suggesting that chlamydia may selectively target the IFN-{gamma} signaling pathways required for MHC class II expression. Chlamydial inhibition of MHC class II expression is correlated with degradation of upstream stimulatory factor (USF)-1, a constitutively and ubiquitously expressed transcription factor required for IFN-{gamma} induction of class II transactivator (CIITA) but not of IRF-1 and ICAM-1. CIITA is an obligate mediator of IFN-{gamma}–inducible MHC class II expression. Thus, diminished CIITA expression as a result of USF-1 degradation may account for the suppression of the IFN-{gamma}–inducible MHC class II in chlamydia-infected cells. These results reveal a novel immune evasion strategy used by the intracellular bacterial pathogen chlamydia that improves our understanding of the molecular basis of pathogenesis.

Key Words: interferon {gamma} induction • major histocompatibility complex class II • chlamydia • upstream stimulatory factor 1 • protein degradation

Address correspondence to Guangming Zhong, Dept. of Medical Microbiology, University of Manitoba, 508-730 William Ave., Winnipeg, Manitoba, Canada R3E OW3. Phone: 204-789-3835; Fax: 204-789-3926; E-mail: gmzhong{at}cc.umanitoba.ca

Abbreviations used: CIITA, class II transactivator; IDO, indoleamine 2,3-dioxygenase; IRF, interferon regulatory factor; JAK, Janus tyrosine kinase; MOI, multiplicity of infection; MOMP, major outer membrane protein; RT, reverse transcriptase; STAT, signal transducers and activators of transcription; USF, upstream stimulatory factor.


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