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This Article Full Text (PDF) All Versions of this Article: jimmunol.0900295v1 183/2/1313    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Gondek, D. C. Articles by Starnbach, M. N. PubMed PubMed Citation Articles by Gondek, D. C. Articles by Starnbach, M. N.

T Cell Responses in the Absence of IFN- Exacerbate Uterine Infection with Chlamydia trachomatis

Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115

Infection with the obligate intracellular bacterium Chlamydia trachomatis is controlled primarily by IFN- and Th1 immunity. In this study, we used cells from a Chlamydia-specific CD4⁺ TCR-transgenic mouse to assess the role of IFN- in development of Th1 immunity. We show that secretion of host IFN- or the ability of host cells to respond to secreted IFN- 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-^–/– recipient mouse demonstrate protective effects, but the same cells exacerbate bacterial burden when transferred into IFN-R^–/– mice. Thus, we demonstrate that the secretion of IFN- is necessary for protection against C. trachomatis and that in the absence of host cell IFN-R expression, both Th1 and Th2 cells lead to increased burden of C. trachomatis.

¹Address correspondence and reprint requests to Dr. Michael N. Starnbach, Department of Microbiology and Molecular Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115. E-mail address: starnbach{at}hms.harvard.edu