T Cell Responses in the Absence of IFN-γ Exacerbate Uterine Infection with Chlamydia trachomatis
| Autor: | Nadia R. Roan, Michael N. Starnbach, David C. Gondek |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Exacerbation
T-Lymphocytes T cell Immunology Chlamydia trachomatis Biology medicine.disease_cause Article Microbiology Interferon-gamma Mice Th2 Cells Uterine infection medicine Animals Immunology and Allergy Secretion Receptors Interferon Mice Knockout Uterine Diseases Chlamydia Obligate Chlamydia Infections Th1 Cells medicine.disease biology.organism_classification medicine.anatomical_structure Female Bacteria |
| Zdroj: | The Journal of Immunology. 183:1313-1319 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.0900295 |
| Popis: | Infection with the obligate intracellular bacterium Chlamydia trachomatis is controlled primarily by IFN-γ and Th1 immunity. In this study, we used cells from a Chlamydia-specific CD4+ TCR-transgenic mouse to assess the role of IFN-γ in development of Th1 immunity. We show that secretion of host IFN-γ or the ability of host cells to respond to secreted IFN-γ 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-γ−/− recipient mouse demonstrate protective effects, but the same cells exacerbate bacterial burden when transferred into IFN-γR−/− mice. Thus, we demonstrate that the secretion of IFN-γ is necessary for protection against C. trachomatis and that in the absence of host cell IFN-γR expression, both Th1 and Th2 cells lead to increased burden of C. trachomatis. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|