Abstract
Genital C. trachomatis infections typically last for many months in women. This has been attributed to several strategies by which C. trachomatis evades immune detection, including well-described methods by which C. trachomatis decreases the cell surface expression of the antigen presenting molecules major histocompatibility complex (MHC) class I, MHC class II, and CD1d in infected genital epithelial cells. We have harnessed new methods that allow for separate evaluation of infected and uninfected cells within a mixed population of chlamydia-infected endocervical epithelial cells to demonstrate that MHC class I downregulation in the presence of C. trachomatis is mediated by direct and indirect (soluble) factors. Such indirect mechanisms may aid in priming surrounding cells for more rapid immune evasion upon pathogen entry and help promote unfettered spread of C. trachomatis genital infections.
Highlights
Chlamydia trachomatis is an obligate intracellular bacterium with a distinctive developmental cycle [1]
We evaluated major histocompatibility complex (MHC) class I surface expression in these two cell populations to determine whether C. trachomatis-associated downregulation of MHC class I occurs in noninfected, but exposed bystander cells
A2EN cells are of endocervical origin and, immortalized, they retain the characteristics of primary human endocervical epithelial cells through multiple passages [12, 18] and can be infected with C. trachomatis
Summary
Chlamydia trachomatis is an obligate intracellular bacterium with a distinctive developmental cycle [1]. Cells were permeabilized, exposed to anti-chlamydial-LPS-FITC and to a fluorescently-labeled antibody recognizing properly folded MHC class I molecules in association with β2-microglobiulin, and analyzed by flow cytometry.
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