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 click here of the host to counter C. trachomatis infection. Genital infections with Chlamydia trachomatis serovars D-K are the most prevalent sexually transmitted bacterial infection (CDC, 2010). The propensity for these intracellular infections to remain relatively asymptomatic in women, combined with the ability of C. trachomatis to survive for extended periods in the genital tract,

make this pathogen a major public health challenge. Although the microorganism is susceptible to antibiotics, asymptomatic patients typically go untreated. Infection that ascends into the upper tract can cause pelvic inflammatory disease that can eventually lead to tubal infertility, ectopic pregnancy, and chronic pelvic pain (Brunham & Rey-Ladino, 2005). Chlamydia trachomatis infection also enhances human immunodeficiency virus acquisition and shedding (Plummer et al., 1991; Ghys et al., 1997) and has been implicated as a cofactor in HPV-induced cervical mafosfamide neoplasia (reviewed in Paavonen, 2011] and possibly preterm Navitoclax in vivo labor (Baud et al., 2008). Co-evolution of C. trachomatis with its human host has driven the acquisition of several immune evasion strategies that likely contribute to the above and promote continued spread of disease (Brunham & Rey-Ladino, 2005). Chlamydia trachomatis is an obligate intracellular pathogen and genital serovars have a tropism for columnar epithelial cells of the female and male genital tracts. When C. trachomatis is recognized by the host immune system, innate [natural killer (NK) cells (Tseng & Rank,

1998; Hook et al., 2004, 2005)]; innate-like [NK T (NKT) cells (Yang, 2007)] and adaptive [CD4+ (Ficarra et al., 2008) and CD8+ T cells (Igietseme et al., 1994; Roan & Starnbach, 2006; Ficarra et al., 2008; Igietseme et al., 2009)] immune constituents contribute to host cellular immune defense and/or host immune pathogenesis. To avert detection by CD8+ and CD4+ cells, genital serovars of C. trachomatis decrease epithelial cell surface expression of major histocompatibility (MHC) class I and class II antigen presenting molecules through the secretion of C. trachomatis Protease-like Activity Factor (CPAF), a chlamydia-encoded protein (Zhong et al., 1999, 2000, 2001; Shaw et al., 2002). CPAF is also involved in the degradation of CD1d, the host cell ligand for NKT cells, in penile genital epithelial cells (Kawana et al., 2007, 2008). While most experiments are conducted using supraphysiologic C.