title: Immunosuppressive effect of progesterone on dendritic cells in mice.
abstract: Progesterone has been demonstrated to be involved in maintaining pregnancy by regulating immunocytes. Dendritic cells (DCs), the most potent triggers of the adaptive immune response, express receptors for steroid hormones and are regarded as one of the primary targets of progesterone. However, the functional modification of DCs by progesterone remains poorly understood. Here, we report that progesterone does not affect the morphology or apoptosis of murine bone marrow-derived DCs. Progesterone-treated DCs were characterized by decreased expression of Ia (MHC class II), CD80 and CD86, increased production of IL-10, and decreased secretion of IL-12. Compared with mature DCs (mDCs), activated progesterone-treated DCs had a reduced capacity to stimulate CD4(+) T cell proliferation. The observation that progesterone-treated DCs could attenuate delayed-type hypersensitivity (DTH) responses in vivo suggests that progesterone mediates suppressive DC activity. However, transfer of progesterone-treated DCs into the peritoneal cavity of mice did not elevate the percentage of CD4(+)CD25(+)Foxp3(+) regulatory T cells in the spleen. Overall, our study helps to increase understanding of the role of DCs exposed to progesterone in the maintenance of pregnancy.
authors.affiliation: Department of Immunology, Taishan Medical University, Taian 271016, Shandong Province, People's Republic of China.
authors.forename: Yingping
authors.initials: Y
authors.lastname: Xu
authors.forename: Hao
authors.initials: H
authors.lastname: He
authors.forename: Chuanwei
authors.initials: C
authors.lastname: Li
authors.forename: Yunzhi
authors.initials: Y
authors.lastname: Shi
authors.forename: Qian
authors.initials: Q
authors.lastname: Wang
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Wengang
authors.initials: W
authors.lastname: Song
mesh_terms: D056704:Adaptive Immunity / Q000276:immunology / Q000502:physiology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology; D018122:B7-1 Antigen / Q000276:immunology; D051940:B7-2 Antigen / Q000276:immunology; D049109:Cell Proliferation / Q000187:drug effects; D003713:Dendritic Cells / Q000166:cytology / Q000276:immunology*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D007108:Immune Tolerance / Q000502:physiology*; D007166:Immunosuppressive Agents / Q000276:immunology* / Q000494:pharmacology; D016753:Interleukin-10 / Q000276:immunology; D018664:Interleukin-12 / Q000276:immunology; D051379:Mice; D008822:Mice, Transgenic; D011247:Pregnancy / Q000276:immunology*; D011374:Progesterone / Q000276:immunology* / Q000494:pharmacology; D011372:Progestins / Q000276:immunology / Q000494:pharmacology; D050378:T-Lymphocytes, Regulatory / Q000166:cytology / Q000276:immunology
chemical_list: D018122:B7-1 Antigen; D051940:B7-2 Antigen; C497965:Cd86 protein, mouse; D000949:Histocompatibility Antigens Class II; C556062:IL10 protein, mouse; D007166:Immunosuppressive Agents; D011372:Progestins; D016753:Interleukin-10; D018664:Interleukin-12; D011374:Progesterone