ArticleFEMS immunology and medical microbiology2012
Modulation of MICA on the surface of Chlamydia trachomatis-infected endocervical epithelial cells promotes NK cell-mediated killing.
Article in FEMS immunology and medical microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- A microphysiologic human cervical model recapitulates microbial, immune, and pathogenic properties of sexually transmitted infections.Science advances · 2026Article
- Interferon-epsilon is a novel regulator of NK cell responses in the uterus.EMBO molecular medicine · 2024Article
- Insights into innate immune cell evasion byFrontiers in immunology · 2024Review
- A Soluble NK-CAR Mediates the Specific Cytotoxicity of NK Cells toward the Target CD20Aging and disease · 2022Article
- Article
- Chlamydia trachomatis-infected cells and uninfected-bystander cells exhibit diametrically opposed responses to interferon gamma.Scientific reports · 2018Article
- Enhanced Direct Major Histocompatibility Complex Class I Self-Antigen Presentation Induced by Chlamydia Infection.Infection and immunity · 2016Article
- Conjunctival scarring in trachoma is associated with the HLA-C ligand of KIR and is exacerbated by heterozygosity at KIR2DL2/KIR2DL3.PLoS neglected tropical diseases · 2014Article
- Article
- Perforin is detrimental to controlling [corrected] C. muridarum replication in vitro, but not in vivo.PloS one · 2013Article
- The major CD8 T cell effector memory subset in the normal and Chlamydia trachomatis-infected human endocervix is low in perforin.BMC immunology · 2012Article
- Elevation of soluble major histocompatibility complex class I related chain A protein in malignant and infectious diseases in Chinese patients.BMC immunology · 2012Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Chlamydia trachomatis serovars D-K are obligate intracellular bacteria that have tropism for the columnar epithelial cells of the genital tract. Chlamydia trachomatis infection has been reported to induce modifications in immune cell ligand expression on epithelial host cells. In this study, we used an in vitro infection model that resulted in a partial infection of C. trachomatis-exposed primary-like immortalized endocervical epithelial cells (A2EN). Using this model, we demonstrated that expression of the natural killer (NK) cell activating ligand, MHC class I-related protein A (MICA), was upregulated on C. trachomatis-infected, but not on noninfected bystander cells. MICA upregulation was concomitant with MHC class I downregulation and impacted the susceptibility of C. trachomatis-infected cells to NK cell activity. The specificity of MICA upregulation was reflected by a higher cytolytic activity of an NK cell line (NK92MI) against C. trachomatis-infected cells compared with uninfected control cells. Significantly, data also indicated that NK cells exerted a partial, but incomplete sterilizing effect on C. trachomatis as shown by the reduction in recoverable inclusion forming units (IFU) when cocultured with C. trachomatis-infected cells. Taken together, our data suggest that NK cells may play a significant role in the ability of the host to counter C. trachomatis infection.
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