Chlamydia, an obligate intracellular bacterial pathogen, can successfully infect a wide range of host species and persist in the infected hosts for a long period of time, suggesting that 'Chlamydia' may have evolved strategies for escaping host defense mechanisms. We have found that ' Chlamydia' indeed possesses the ability to evade host immune recognition. Immune recognition is a requirement for hosts to develop an effective immunity against microbial infections. It has been shown that MHC class II-mediated immune responses often play a critical role in controlling intracellular pathogen infection. We hypothesized that 'Chlamydia' may suppress MHC class II expression in order to escape MHC class II-mediated immune responses. We compared the IFN--inducible MHC class II expression between epithelial cells with or without chlamydial infection. In conclusion, the selective inhibition of IFN--inducible MHC class II, but not ICAM-1, by chlamydial infection may be driven by host immune selective pressure. (Abstract shortened by UMI.)