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10.1038/cddis.2017.95 http://scihub22266oqcxt.onion/10.1038/cddis.2017.95 C5386585!5386585 !28300844     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28300844 &cmd=llinks): Failed to open stream: HTTP request failed! 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IL-27 triggers IL-10 production in Th17 cells via a c-Maf/ROR?t/Blimp-1 signal to promote the progression of endometriosis |pdf=|usr=}}{{28300844 }} gab.com Text IL-27 triggers IL-10 production in Th17 cells via a c-Maf/ROR t/Blimp-1 signal to promote the progression of endometriosis JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28300844 #FOAvip Endometriosis is an estrogen-dependent inflammatory disease. The anti-inflammatory cytokine IL-10 is also increased in endometriosis. IL-10 production by Th17 cells is critical for limiting autoimmunity and inflammatory responses. However, the mechanism of inducing IL-10-producing Th17 cells is still largely unknown. The present study investigated the differentiation mechanism and role of IL-10-producing Th17 cells in endometriosis. Here, we report that IL-10(+)Th17 cells are significantly increased in the peritoneal fluid of women with endometriosis, along with an elevation of IL-27, IL-6 and TGF-?. Compared with peripheral CD4(+) T cells, endometrial CD4(+) T cells highly expressed IL-27 receptors, especially the ectopic endometrium. Under external (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) and local (estrogen, IL-6 and TGF-?) environmental regulation, IL-27 from macrophages and endometrial stromal cells (ESCs) induces IL-10 production in Th17 cells in vitro and in vivo. This process may be mediated through the interaction between c-musculoaponeurotic fibrosarconna (c-Maf) and retinoic acid-related orphan receptor gamma t (ROR?t), and associated with the upregulation of downstream B lymphocyte-induced maturation protein-1 (Blimp-1). IL-10(+)Th17 cells, in turn, stimulate the proliferation and implantation of ectopic lesions and accelerate the progression of endometriosis. These results suggest that IL-27 is a pivotal regulator in endometriotic immune tolerance by triggering Th17 cells to produce IL-10 and promoting the rapid growth and implantation of ectopic lesions. This finding provides a scientific basis for potential therapeutic strategies aimed at preventing the development of endometriosis, especially for patients with high levels of IL-10(+)Th17 cells. Twit Text FOAVip IL-27 triggers IL-10 production in Th17 cells via a c-Maf/ROR t/Blimp-1 signal to promote the progression of endometriosis ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28300844 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28300844 #FOAvip English Wikipedia <ref>{{Cite pmid|28300844 }}</ref> IL-27 triggers IL-10 production in Th17 cells via a c-Maf/ROR?t/Blimp-1 signal to promote the progression of endometriosis #MMPMID28300844 Chang KK ; Liu LB ; Jin LP ; Zhang B ; Mei J ; Li H ; Wei CY ; Zhou WJ ; Zhu XY ; Shao J ; Li DJ ; Li MQ Cell Death Dis 2017[Mar]; 8 (3 ): e2666 PMID28300844 show ga Endometriosis is an estrogen-dependent inflammatory disease. The anti-inflammatory cytokine IL-10 is also increased in endometriosis. IL-10 production by Th17 cells is critical for limiting autoimmunity and inflammatory responses. However, the mechanism of inducing IL-10-producing Th17 cells is still largely unknown. The present study investigated the differentiation mechanism and role of IL-10-producing Th17 cells in endometriosis. Here, we report that IL-10(+)Th17 cells are significantly increased in the peritoneal fluid of women with endometriosis, along with an elevation of IL-27, IL-6 and TGF-?. Compared with peripheral CD4(+) T cells, endometrial CD4(+) T cells highly expressed IL-27 receptors, especially the ectopic endometrium. Under external (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) and local (estrogen, IL-6 and TGF-?) environmental regulation, IL-27 from macrophages and endometrial stromal cells (ESCs) induces IL-10 production in Th17 cells in vitro and in vivo. This process may be mediated through the interaction between c-musculoaponeurotic fibrosarconna (c-Maf) and retinoic acid-related orphan receptor gamma t (ROR?t), and associated with the upregulation of downstream B lymphocyte-induced maturation protein-1 (Blimp-1). IL-10(+)Th17 cells, in turn, stimulate the proliferation and implantation of ectopic lesions and accelerate the progression of endometriosis. These results suggest that IL-27 is a pivotal regulator in endometriotic immune tolerance by triggering Th17 cells to produce IL-10 and promoting the rapid growth and implantation of ectopic lesions. This finding provides a scientific basis for potential therapeutic strategies aimed at preventing the development of endometriosis, especially for patients with high levels of IL-10(+)Th17 cells. |Adult [MESH] |CD4-Positive T-Lymphocytes/metabolism/pathology [MESH] |Cell Differentiation/physiology [MESH] |Disease Progression [MESH] |Endometriosis/*metabolism/pathology [MESH] |Endometrium/metabolism/pathology [MESH] |Female [MESH] |Humans [MESH] |Interleukin-10/*metabolism [MESH] |Interleukin-6/metabolism [MESH] |Interleukins/*metabolism [MESH] |Macrophages/metabolism/pathology [MESH] |Nuclear Receptor Subfamily 1, Group F, Member 3/*metabolism [MESH] |Positive Regulatory Domain I-Binding Factor 1 [MESH] |Proto-Oncogene Proteins c-maf/*metabolism [MESH] |Repressor Proteins/*metabolism [MESH] |Stromal Cells/metabolism/pathology [MESH] |Th17 Cells/*metabolism [MESH] |Transforming Growth Factor beta/metabolism [MESH]IL-27 triggers IL-10 production in Th17 cells via a c-Maf/ROR?t/Blimp-(epmc).pdf DeepDyve Pubget Overpricing