The Journal of Experimental Medicine
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Published online 1 May 2000.
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© The Rockefeller University Press, 0022-1007/2000/5/1525/ $5.00
The Journal of Experimental Medicine, Volume 191, Number 9, May 1, 2000 1525-1534

Original Article

Degradation of Transcription Factor Rfx5 during the Inhibition of Both Constitutive and Interferon {gamma}–Inducible Major Histocompatibility Complex Class I Expression in Chlamydia-Infected Cells

Guangming Zhonga, Li Liua, Tao Fana, Peiyi Fana, and Hezhao Jia

a From the Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba R3E OW3, Canada
Dept. of Microbiology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curve Dr., San Antonio, TX 78284-7758.210-567-6612210-567-1169

zhongg{at}uthscsa.edu

We have previously shown that the obligate intracellular pathogen chlamydia can suppress interferon (IFN)-{gamma}–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-{gamma}–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-{gamma}–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.

Key Words: MHC class I suppression • RFX5 degradation • IFN-{gamma} induction • chlamydial infection • proteasomal activity

Abbreviations used in this paper: β2M, β2-microglobulin; CPA, chlamydia-dependent proteasome-like activity; CIITA, class II transactivator; EndoH, endoglycosidase H; MOI, multiplicity of infection; MOMP, major outer membrane protein; RT, reverse transcriptase; STAT, signal transducer and activator of transcription; TPP2, tripeptidyl peptidase II; USF, upstream stimulation factor.

© 2000 The Rockefeller University Press


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