|
|
|
|
|
|
|
||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
J. Exp. Med.,
Volume 189, Number 12, June 21, 1999 1931-1938
-inducible Major
Histocompatibility Complex Class II Expression by
Degradation of Upstream Stimulatory Factor 1
By
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)-
-inducible major histocompatibility complex (MHC) class II expression.
However, the IFN--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- 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- induction of class II transactivator (CIITA) but not of IRF-1 and ICAM-1. CIITA is an obligate mediator
of IFN--inducible MHC class II expression. Thus, diminished CIITA expression as a result of
USF-1 degradation may account for the suppression of the IFN--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.
induction;
major histocompatibility complex class II;
chlamydia;
upstream stimulatory factor 1;
protein degradation
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
| TABLE OF CONTENTS |
|
