T cell responses in the absence of IFN-gamma exacerbate uterine infection with Chlamydia trachomatis

J Immunol. 2009 Jul 15;183(2):1313-9. doi: 10.4049/jimmunol.0900295. Epub 2009 Jun 26.

Abstract

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.

MeSH terms

  • Animals
  • Chlamydia Infections / immunology*
  • Chlamydia trachomatis*
  • Female
  • Interferon-gamma / deficiency
  • Interferon-gamma / immunology*
  • Mice
  • Mice, Knockout
  • Receptors, Interferon / deficiency
  • Receptors, Interferon / immunology*
  • T-Lymphocytes / immunology*
  • Th1 Cells / immunology
  • Th2 Cells
  • Uterine Diseases / microbiology*

Substances

  • Receptors, Interferon
  • interferon gamma receptor
  • Interferon-gamma