Exploring the antigen-specific memory CD4 T cell response to Chlamydia female reproductive tract reinfection

Abstract

Abstract Chlamydia is now the most commonly reported infectious disease in the United States and more than 3 million new cases occur annually. Despite numerous attempts made by researchers to develop a vaccine strategy over the past two decades, to date, no Chlamydia vaccine is available. Among all immunization strategies tested in mouse models of Chlamydia infection, none generates protective immunity any better than a naturally resolved prior Chlamydia female reproductive tract (FRT) infection. Research in our laboratory aims to understand how immunological memory shaped by a natural episode of Chlamydia primary infection confer such potent protective immunity. Using Chlamydia-specific MHC Class II tetramers, our preliminary studies show that Chlamydia secondary infection induced massive clonal expansion of antigen-specific CD4 T cells in the FRT seven days post reinfection. In contrast, a robust recall response is not observed in local draining lymph nodes or spleen at any time point post challenge. Surprisingly, Chlamydia-specific memory CD4 T cells in the FRT do not express a common marker for tissue-resident T cells, CD69. We are now focusing our efforts on understanding the activation, effector function, and maintenance of Chlamydia-specific memory CD4 T cells in the FRT during Chlamydia reinfection.