ArticleInfection and immunity2002
Role of interferon-stimulated gene factor 3gamma and beta interferon in HLA class I enhancement in synovial fibroblasts upon infection with Chlamydia trachomatis.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- Large Screening Identifies ACE2 Positively Correlates With NF-κB Signaling Activity and Targeting NF-κB Signaling Drugs Suppress ACE2 Levels.Frontiers in pharmacology · 2021Article
- Chlamydia trachomatis-infected epithelial cells and fibroblasts retain the ability to express surface-presented major histocompatibility complex class I molecules.Infection and immunity · 2014Article
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chlamydia trachomatis infection can cause reactive arthritis that is associated with the persistence of chlamydial organisms in the joint. Fibroblasts of the synovial membrane represent host cells for Chlamydia during articular infection. In this study we investigated the expression of HLA class I molecules in synovial fibroblasts following infection with C. trachomatis D. The expression of HLA class I heavy chain (HLA-I) was up-regulated in infected cultures as shown by reverse transcription-PCR and immunoblotting. The increase in cell surface expression of HLA-I and beta(2) microglobulin on infected fibroblasts was demonstrated by flow cytometric analysis. Suppression of enhanced production of interferon-stimulated gene factor 3gamma (ISGF3gamma) in infected cell cultures by antisense oligonucleotide treatment reduced the level of HLA-I. Blocking antibodies to beta interferon (IFN-beta) inhibited the Chlamydia-induced enhancement of both ISGF3gamma and HLA-I. These findings show that the up-regulation of HLA-I in synovial fibroblasts infected with C. trachomatis is caused by the induction of IFN-beta, which in turn stimulates the synthesis of ISGF3gamma, a transcription factor participating in the regulation of the HLA-I gene. The IFN-beta-mediated expression of HLA-I on Chlamydia-infected cells may be a regulatory factor in the immune response in chlamydial infections.
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Registered trials
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