Modulation of MICA on the surface of Chlamydia trachomatis-infected endocervical epithelial cells promotes NK cell-mediated killing.

Autor: Ibana JA; Department of Microbiology, Immunology and Parasitology, Louisiana State University Health Science Center, New Orleans, LA, USA., Aiyar A, Quayle AJ, Schust DJ
Jazyk: angličtina
Zdroj: FEMS immunology and medical microbiology [FEMS Immunol Med Microbiol] 2012 Jun; Vol. 65 (1), pp. 32-42. Date of Electronic Publication: 2012 Feb 16.
DOI: 10.1111/j.1574-695X.2012.00930.x
Abstrakt: 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.
(© 2012 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved.)
Databáze: MEDLINE
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