Chlamydia trachomatis is a major cause of sexually transmitted disease in this country including both mucosal infection and invasive disease (such as pneumonia in infants). Despite its importance, the important host defense mechanisms against C. trachomatis infection are poorly defined. Our previous studies employing a murine model of pneumonia due to the mouse pneumonitis agent (MoPn, a murine biovar of C. trachomatis) have implicated both antibody and cell-mediated immunity (CMI) as important in control of MoPn infection. This project will define the role of nunhumoral immunity in host defense against MoPn. To define the role of CMI, beige mice (which produce antibody normally but have impaired cytotoxic function) will be employed. Further, the B cell-deficient mouse (treated with anti-mu antibody from birth) will be used to further define the role of CMI in host resistance to MoPn. As before, we will also employ the nude (athymic, T cell-deficient) mouse and its heterozygous littermates. Specific parameters of CMI in host defense against MoPn to be explored will include the macrophage, natural killer cells, cytotoxic T cells, and lymphokines (particularly interferon and interleukin-2). Mechanisms of control of MoPn replication within epithelial cells (the natural host cell) by lymphokines will be examined. These studies will provide needed data on the important mechanisms of CMI in host defense against C. trachomatis.
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