Degradation of transcription factor RFX5 during the inhibition of both constitutive and interferon γ-inducible major histocompatibility complex class I expression in chlamydia-infected cells

Guangming Zhong, Li Liu, Tao Fan, Peiyi Fan, Hezhao Ji

Research output: Contribution to journalArticle

165 Scopus citations

Abstract

We have previously shown that the obligate intracellular pathogen chlamydia can suppress interferon (IFN)-γ-inducible major histocompatibility complex (MHC) class II expression in infected cells by degrading upstream stimulation factor (USF)-1. We now report that chlamydia can also inhibit both constitutive and IFN-γ-inducible MHC class I expression in the infected cells. The inhibition of MHC class I molecule expression correlates well with degradation of RFX5, an essential downstream transcription factor required for both the constitutive and IFN-γ-inducible MHC class I expression. We further demonstrate that a lactacystin-sensitive proteasome-like activity identified in chlamydia-infected cell cytosolic fraction can degrade both USF-1 and RFX5. This proteasome-like activity is dependent on chlamydial but not host protein synthesis. Host preexisting proteasomes may not be required for the unique proteasome-like activity. These observations suggest that chlamydia-secreted factors may directly participate in the proteasome-like activity. Efforts to identify the chlamydial factors are underway. These findings provide novel information on the molecular mechanisms of chlamydial evasion of host immune recognition.

Original languageEnglish (US)
Pages (from-to)1525-1534
Number of pages10
JournalJournal of Experimental Medicine
Volume191
Issue number9
DOIs
StatePublished - May 1 2000

Keywords

  • Chlamydial infection
  • IFN-γ induction
  • MHC class I suppression
  • Proteasomal activity
  • RFX5 degradation

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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