期刊
JOURNAL OF IMMUNOLOGY
卷 183, 期 2, 页码 1313-1319出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0900295
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资金
- NIAID NIH HHS [F32 AI081429-01A1, R01 AI039558-09, R01 AI039558-08, F32 AI081429, T32 AI007061, R01 AI039558-06, R01 AI039558-07, R01 AI039558] Funding Source: Medline
Infection with the obligate intracellular bacterium Chlamydia trachomatis is controlled primarily by IFN-gamma and Th1 immunity. In this study, we used cells from a Chlamydia-specific CD4(+) TCR-transgenic mouse to assess the role of IFN-gamma in development of Th1 immunity. We show that secretion of host IFN-gamma or the ability of host cells to respond to secreted IFN-gamma is not required to initiate a Th1 immune response. Additionally, we found that Ag-specific CD4(+) cells that were preskewed toward Th1 confer protection, whereas cells preskewed toward Th2 cause a previously unreported exacerbation of disease leading to higher bacterial load. Chlamydia-specific Th1 cells transferred into an IFN-gamma(-/-) recipient mouse demonstrate protective effects, but the same cells exacerbate bacterial burden when transferred into IFN-gamma R-/- mice. Thus, we demonstrate that the secretion of IFN-gamma is necessary for protection against C. trachomatis and that in the absence of host cell IFN-gamma R expression, both Th1 and Th2 cells lead to increased burden of C. trachomatis. The Journal of Immunology, 2009, 183: 1313-1319.
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