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

We report that chlamydiae, which are obligate intracellular bacterial pathogens, can inhibit interferon (IFN)-γ–inducible major histocompatibility complex (MHC) class II expression. However, the IFN-γ–induced IFN regulatory factor-1 (IRF-1) and intercellular adhesion molecule 1 (ICAM-1) expression i...

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Main Authors:	Zhong, Guangming, Fan, Tao, Liu, Li
Format:	Online
Language:	English
Published:	The Rockefeller University Press 1999
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192973/

id	pubmed-2192973
recordtype	oai_dc
spelling	pubmed-21929732008-04-16 Chlamydia Inhibits Interferon γ–inducible Major Histocompatibility Complex Class II Expression by Degradation of Upstream Stimulatory Factor 1 Zhong, Guangming Fan, Tao Liu, Li Articles We report that chlamydiae, which are obligate intracellular bacterial pathogens, can inhibit interferon (IFN)-γ–inducible major histocompatibility complex (MHC) class II expression. However, the IFN-γ–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-γ 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-γ induction of class II transactivator (CIITA) but not of IRF-1 and ICAM-1. CIITA is an obligate mediator of IFN-γ–inducible MHC class II expression. Thus, diminished CIITA expression as a result of USF-1 degradation may account for the suppression of the IFN-γ–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. The Rockefeller University Press 1999-06-21 /pmc/articles/PMC2192973/ /pubmed/10377188 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Zhong, Guangming Fan, Tao Liu, Li
spellingShingle	Zhong, Guangming Fan, Tao Liu, Li Chlamydia Inhibits Interferon γ–inducible Major Histocompatibility Complex Class II Expression by Degradation of Upstream Stimulatory Factor 1
author_facet	Zhong, Guangming Fan, Tao Liu, Li
author_sort	Zhong, Guangming
title	Chlamydia Inhibits Interferon γ–inducible Major Histocompatibility Complex Class II Expression by Degradation of Upstream Stimulatory Factor 1
title_short	Chlamydia Inhibits Interferon γ–inducible Major Histocompatibility Complex Class II Expression by Degradation of Upstream Stimulatory Factor 1
title_full	Chlamydia Inhibits Interferon γ–inducible Major Histocompatibility Complex Class II Expression by Degradation of Upstream Stimulatory Factor 1
title_fullStr	Chlamydia Inhibits Interferon γ–inducible Major Histocompatibility Complex Class II Expression by Degradation of Upstream Stimulatory Factor 1
title_full_unstemmed	Chlamydia Inhibits Interferon γ–inducible Major Histocompatibility Complex Class II Expression by Degradation of Upstream Stimulatory Factor 1
title_sort	chlamydia inhibits interferon γ–inducible major histocompatibility complex class ii expression by degradation of upstream stimulatory factor 1
description	We report that chlamydiae, which are obligate intracellular bacterial pathogens, can inhibit interferon (IFN)-γ–inducible major histocompatibility complex (MHC) class II expression. However, the IFN-γ–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-γ 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-γ induction of class II transactivator (CIITA) but not of IRF-1 and ICAM-1. CIITA is an obligate mediator of IFN-γ–inducible MHC class II expression. Thus, diminished CIITA expression as a result of USF-1 degradation may account for the suppression of the IFN-γ–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.
publisher	The Rockefeller University Press
publishDate	1999
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192973/
_version_	1611430812357492736

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

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