ArticleThe Journal of experimental medicine2000
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.
Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 196 citations in OpenAlex.
- Irradiated whole cell Chlamydia vaccine confers significant protection in a murine genital tract challenge model.NPJ vaccines · 2024Article
- IgG exacerbates genital chlamydial pathology in females by enhancing pathogenic CD8Scandinavian journal of immunology · 2024Article
- Clinical significance and prognostic role of an immune-related gene signature in gastric adenocarcinoma.Aging · 2021Article
- Article
- Modeling of variables in cellular infection reveals CXCL10 levels are regulated by human genetic variation and the Chlamydia-encoded CPAF protease.Scientific reports · 2020Article
- Human Fallopian Tube Epithelial Cell Culture Model To Study Host Responses to Chlamydia trachomatis Infection.Infection and immunity · 2020Article
- Article
- Fighting Persistence: How Chronic Infections with Mycobacterium tuberculosis Evade T Cell-Mediated Clearance and New Strategies To Defeat Them.Infection and immunity · 2020Review
- Review
- An Ancient Molecular Arms Race:Frontiers in immunology · 2020Review
- The multiple functions of the numerousMicrobial cell (Graz, Austria) · 2019Review
- TLR3 deficiency exacerbates the loss of epithelial barrier function during genital tract Chlamydia muridarum infection.PloS one · 2019Article
- Review
- Chlamydia trachomatis-infected cells and uninfected-bystander cells exhibit diametrically opposed responses to interferon gamma.Scientific reports · 2018Article
- The Chlamydia-Secreted Protease CPAF Promotes Chlamydial Survival in the Mouse Lower Genital Tract.Infection and immunity · 2016Article
- Enhanced Direct Major Histocompatibility Complex Class I Self-Antigen Presentation Induced by Chlamydia Infection.Infection and immunity · 2016Article
- Characterization of CPAF critical residues and secretion during Chlamydia trachomatis infection.Infection and immunity · 2015Article
- Induction and inhibition of CPAF activity during analysis of Chlamydia-infected cells.Pathogens and disease · 2015Article
- The Chlamydia protease CPAF: caution, precautions and function.Pathogens and disease · 2014Article
- Reassessing the role of the secreted protease CPAF in Chlamydia trachomatis infection through genetic approaches.Pathogens and disease · 2014Article
28 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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