the female lower genital tract is a privileged compartment with il-10 producing dendritic cells and poor th1 immunity following chlamydia trachomatis infection女性下生殖道是一个特权舱与树突细胞产生il - 10和穷人th1沙眼衣原体感染后免疫.pdfVIP
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the female lower genital tract is a privileged compartment with il-10 producing dendritic cells and poor th1 immunity following chlamydia trachomatis infection女性下生殖道是一个特权舱与树突细胞产生il - 10和穷人th1沙眼衣原体感染后免疫
The Female Lower Genital Tract Is a Privileged
Compartment with IL-10 Producing Dendritic Cells and
Poor Th1 Immunity following Chlamydia trachomatis
Infection
¤
Ellen Marks, Miguel A. Tam , Nils Y. Lycke*
Department of Microbiology and Immunology, Mucosal Immunobiology and Vaccine Center, Institute of Biomedicine, The University of Gothenburg, Gothenburg,
Sweden
Abstract
While a primary genital tract infection with C. trachomatis stimulates partial-protection against re-infection, it may also result in
severe inflammation and tissue destruction. Here we have dissected whether functional compartments exist in the genital
tract that restrict Th1-mediated protective immunity. Apart from the Th1-subset, little is known about the role of other CD4+ T
cell subsets in response to a genital tract chlamydial infection. Therefore, we investigated CD4+ T cell subset differentiation in
the genital tract using RT-PCR for expression of critical transcription factors and cytokines in the upper (UGT) and lower genital
tract (LGT) of female C57BL/6 mice in response to C. trachomatis serovar D infection. We found that the Th1 subset dominated
the UGT, as IFN-c and T-bet mRNA expression were high, while GATA-3 was low following genital infection with C. trachomatis
serovar D. By contrast, IL-10 and GATA-3 mRNA dominated the LGT, suggesting the presence of Th2 cells. These functional
compartments also attracted regulatory T cells (Tregs) differently as increased FoxP3 mRNA expression was seen primarily in
the UGT. Although IL-17A mRNA was somewhat up-regulated in the LGT, no significant change in RORc-t mRNA expression
was observed, suggesting no involvement of Th17 cells. The dichotomy between the LGT and UGT was maintained during
infection by IL-10 because in IL-10-deficient mice the distinction between the two compartments w
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