ArticleThe Journal of experimental medicine1999
Chlamydia inhibits interferon gamma-inducible major histocompatibility complex class II expression by degradation of upstream stimulatory factor 1.
Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 198 citations in OpenAlex.
- Review
- Comparative transcriptomic profiling of human conjunctival epithelial cells and macrophages in response toFrontiers in cellular and infection microbiology · 2026Article
- Review
- Irradiated whole cell Chlamydia vaccine confers significant protection in a murine genital tract challenge model.NPJ vaccines · 2024Article
- The NLR family of innate immune and cell death sensors.Immunity · 2024Review
- Gynecological Cancers and Microbiota Dynamics: Insights into Pathogenesis and Therapy.International journal of molecular sciences · 2024Review
- Insights into innate immune cell evasion byFrontiers in immunology · 2024Review
- IgG exacerbates genital chlamydial pathology in females by enhancing pathogenic CD8Scandinavian journal of immunology · 2024Article
- The Immunological Synapse: An Emerging Target for Immune Evasion by Bacterial Pathogens.Frontiers in immunology · 2022Review
- Article
- Why do intestinal epithelial cells express MHC class II?Immunology · 2021Review
- The MHC Class II Transactivator CIITA: Not (Quite) the Odd-One-Out Anymore among NLR Proteins.International journal of molecular sciences · 2021Review
- Article
- A novel protein upstream stimulatory factor 2 identified in lamprey, Lethenteron reissneri.Development genes and evolution · 2020Article
- Human Fallopian Tube Epithelial Cell Culture Model To Study Host Responses to Chlamydia trachomatis Infection.Infection and immunity · 2020Article
- Fighting Persistence: How Chronic Infections with Mycobacterium tuberculosis Evade T Cell-Mediated Clearance and New Strategies To Defeat Them.Infection and immunity · 2020Review
- 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
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We report that chlamydiae, which are obligate intracellular bacterial pathogens, can inhibit interferon (IFN)-gamma-inducible major histocompatibility complex (MHC) class II expression. However, the IFN-gamma-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-gamma 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-gamma induction of class II transactivator (CIITA) but not of IRF-1 and ICAM-1. CIITA is an obligate mediator of IFN-gamma-inducible MHC class II expression. Thus, diminished CIITA expression as a result of USF-1 degradation may account for the suppression of the IFN-gamma-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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.