IL-27 Triggers IL-10 Production in Th17 Cell by c-Maf/RORγt/Blimp-1 Signal to Promote the Progress of Endometriosis
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- 英文论文题名：IL-27 Triggers IL-10 Production in Th17 Cell by c-Maf/RORγt/Blimp-1 Signal to Promote the Progress of Endometriosis
- 论文作者：Li Ming-Qing ; Chang Kai-Kai ; Zhou Wen-Jie ; Yang Hui-Li ; Jin Li-Ping ; Li Da-Jin
- 英文论文作者：Li Ming-Qing ; Chang Kai-Kai ; Zhou Wen-Jie ; Yang Hui-Li ; Jin Li-Ping ; Li Da-Jin ; Laboratory for Reproductive Immunology ; Hospital of Obstetrics and Gynecology ; Fudan University ; Clinical and Translational Research Center ; Shanghai First Maternity and Infant Hospital ; Tongji University School of Medicine
- 年：2016
- 作者机构：Laboratory for Reproductive Immunology,Hospital of Obstetrics and Gynecology,Fudan University;Clinical and Translational Research Center,Shanghai First Maternity and Infant Hospital,Tongji University School of Medicine;
- 英文论文关键词：IL-27 ; IL-10~+Th17 ; endometriosis ; c-Maf ; RORγt ; Blimp-1
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会壁报交流集
- 英文会议录名称：Proceedings of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R711.71
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：2
- 文件大小：385k
- 原文格式：D
- 会议级别：全国
摘要
Endometriosis is an estrogen-dependent inflammatory disease.The anti-inflammatory cytokine IL-10 also increased in endometriosis.However,the mechanism for origination and role of IL-10 in endometriosis was still large unknown.Here we report IL-10~+Th17 cells are significantly increased in the peritoneal fluid of women with endometriosis,along with elevation of IL-27,IL-6 and TGF-β.Compared to peripheral CD4~+ T,endometrial CD4~+T highly expressed IL-27 receptors,especially ectopic endometrium.Under external(2,3,7,8-tetrachlorodibenzo-p-dioxin,TCDD) and local(estrogen,IL-6 and TGF-β) environmental regulation,IL-27 from macrophage and endometrial stromal cells(ESC) induces IL-10 produce in Th17 cells in vitro and in vivo.This process is mediated through the interaction between c-musculoaponeuroticfibrosarconma(c-Maf) and retinoic acid-related orphan receptor gamma t(RORγt),and associated with the up-regulation of downstream B lymphocyte-induced maturation protein-1(Blimp-1).Such IL-10~+Th17 cells in turn stimulate the proliferation and implantation of ectopic lesion and accelerate the progress of endometriosis.These results suggest that IL-27 is a pivotal regulator in endometriotic immune tolerance by triggering Th17 to produce IL-10 and promote rapid growth and implantation of ectopic lesion.This provides a scientific basis on which potential therapeutic strategies targeted to prevent the development of endometriosis,especially for patient with high level of IL-10~+Th17 cells.
Endometriosis is an estrogen-dependent inflammatory disease.The anti-inflammatory cytokine IL-10 also increased in endometriosis.However,the mechanism for origination and role of IL-10 in endometriosis was still large unknown.Here we report IL-10~+Th17 cells are significantly increased in the peritoneal fluid of women with endometriosis,along with elevation of IL-27,IL-6 and TGF-β.Compared to peripheral CD4~+ T,endometrial CD4~+T highly expressed IL-27 receptors,especially ectopic endometrium.Under external(2,3,7,8-tetrachlorodibenzo-p-dioxin,TCDD) and local(estrogen,IL-6 and TGF-β) environmental regulation,IL-27 from macrophage and endometrial stromal cells(ESC) induces IL-10 produce in Th17 cells in vitro and in vivo.This process is mediated through the interaction between c-musculoaponeuroticfibrosarconma(c-Maf) and retinoic acid-related orphan receptor gamma t(RORγt),and associated with the up-regulation of downstream B lymphocyte-induced maturation protein-1(Blimp-1).Such IL-10~+Th17 cells in turn stimulate the proliferation and implantation of ectopic lesion and accelerate the progress of endometriosis.These results suggest that IL-27 is a pivotal regulator in endometriotic immune tolerance by triggering Th17 to produce IL-10 and promote rapid growth and implantation of ectopic lesion.This provides a scientific basis on which potential therapeutic strategies targeted to prevent the development of endometriosis,especially for patient with high level of IL-10~+Th17 cells.
Endometriosis is an estrogen-dependent inflammatory disease.The anti-inflammatory cytokine IL-10 also increased in endometriosis.However,the mechanism for origination and role of IL-10 in endometriosis was still large unknown.Here we report IL-10~+Th17 cells are significantly increased in the peritoneal fluid of women with endometriosis,along with elevation of IL-27,IL-6 and TGF-β.Compared to peripheral CD4~+ T,endometrial CD4~+T highly expressed IL-27 receptors,especially ectopic endometrium.Under external(2,3,7,8-tetrachlorodibenzo-p-dioxin,TCDD) and local(estrogen,IL-6 and TGF-β) environmental regulation,IL-27 from macrophage and endometrial stromal cells(ESC) induces IL-10 produce in Th17 cells in vitro and in vivo.This process is mediated through the interaction between c-musculoaponeuroticfibrosarconma(c-Maf) and retinoic acid-related orphan receptor gamma t(RORγt),and associated with the up-regulation of downstream B lymphocyte-induced maturation protein-1(Blimp-1).Such IL-10~+Th17 cells in turn stimulate the proliferation and implantation of ectopic lesion and accelerate the progress of endometriosis.These results suggest that IL-27 is a pivotal regulator in endometriotic immune tolerance by triggering Th17 to produce IL-10 and promote rapid growth and implantation of ectopic lesion.This provides a scientific basis on which potential therapeutic strategies targeted to prevent the development of endometriosis,especially for patient with high level of IL-10~+Th17 cells.
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