| First Author | Gondek DC | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 2 | Pages | 1313-9 |
| PubMed ID | 19561106 | Mgi Jnum | J:151656 |
| Mgi Id | MGI:4354696 | Doi | 10.4049/jimmunol.0900295 |
| Citation | Gondek DC, et al. (2009) T cell responses in the absence of IFN-gamma exacerbate uterine infection with Chlamydia trachomatis. J Immunol 183(2):1313-9 |
| abstractText | 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-gammaR(-/-) 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-gammaR expression, both Th1 and Th2 cells lead to increased burden of C. trachomatis. |
