Abstract
Chlamydia trachomatis infection is the most common bacterial sexually transmitted disease in the United States. Repeated infections with C. trachomatis lead to serious sequelae, such as infertility. It is unclear why the adaptive immune system, specifically the CD8(+) T cell response, is unable to protect against subsequent C. trachomatis infections. In this article, we characterize the mucosal CD8(+) T cell response to C. trachomatis in the murine genital tract. We demonstrate that the immunoinhibitory ligand, PD-L1, contributes to the defective CD8(+) T cell response. Deletion or inhibition of PD-L1 restores the CD8(+) T cell response and enhances C. trachomatis clearance.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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B7-1 Antigen / immunology
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B7-H1 Antigen / deficiency
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B7-H1 Antigen / physiology*
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CD8-Positive T-Lymphocytes / immunology*
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Cervix Uteri / immunology*
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Cervix Uteri / microbiology
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Chlamydia Infections / immunology*
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Chlamydia trachomatis / immunology*
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Female
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Genital Diseases, Female / immunology*
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Genital Diseases, Female / microbiology
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Hematopoietic Stem Cells / immunology
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Immune Tolerance / immunology
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Immunity, Mucosal / immunology*
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Mice
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Mice, Inbred C57BL
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Mucous Membrane / immunology
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Radiation Chimera
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T-Lymphocyte Subsets / immunology*
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Uterus / immunology*
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Uterus / microbiology
Substances
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B7-1 Antigen
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B7-H1 Antigen
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Cd274 protein, mouse