Resolution of secondary Chlamydia trachomatis genital tract infection in immune mice with depletion of both CD4+ and CD8+ T cells.
The essential role of T cells in the resolution of primary murine Chlamydia trachomatis genital tract infection is inarguable; however, much less is known about the mechanisms that confer resistance to reinfection. We previously established that CD4+ T cells and B cells contribute importantly to resistance to reinfection. In our current studies, we demonstrate that immune mice concurrently depleted of both CD4+ T cells and CD8+ T cells resisted reinfection as well as immunocompetent wild-type mice. The in vivo depletion of CD4+ and CD8+ T cells resulted in diminished chlamydia-specific delayed-type hypersensitivity responses, but antichlamydial antibody responses were unaffected. Our data indicate that immunity to chlamydial genital tract reinfection does not rely solely upon immune CD4+ or CD8+ T cells and further substantiate a predominant role for additional effector immune responses, such as B cells, in resistance to chlamydial genital tract reinfection.
Department of Microbiology, Montana State University, Bozeman, Montana 59717, USA.
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D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000502:physiology*; D018414:CD8-Positive T-Lymphocytes / Q000502:physiology*; D002690:Chlamydia Infections / Q000276:immunology*; D002692:Chlamydia trachomatis; D005260:Female; D005831:Genital Diseases, Female / Q000276:immunology*; D006367:HeLa Cells; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000209:etiology; D008212:Lymphocyte Depletion; D051379:Mice; D008810:Mice, Inbred C57BL