Integrin CD11b attenuates colitis by strengthening Src-Akt pathway to polarize anti-inflammatory IL-10 expression
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- 英文论文题名：Integrin CD11b attenuates colitis by strengthening Src-Akt pathway to polarize anti-inflammatory IL-10 expression
- 论文作者：Xiang Hu ; Kewei Qin ; Hua Zhang ; Tianliang Li ; Nan Li ; Xuetao Cao ; Chaofeng Han
- 英文论文作者：Xiang Hu ; Kewei Qin ; Hua Zhang ; Tianliang Li ; Nan Li ; Xuetao Cao ; Chaofeng Han ; National Key Laboratory of Medical Molecular Biology & Department of Immunology ; Institute of Basic Medical Sciences ; Peking Union Medical College ; Chinese Academy of Medical Sciences ; National Key Laboratory of Medical Immunology & Institute of Immunology ; Second Military Medical University
- 年：2016
- 作者机构：National Key Laboratory of Medical Molecular Biology & Department of Immunology,Institute of Basic Medical Sciences,Peking Union Medical College,Chinese Academy of Medical Sciences;National Key Laboratory of Medical Immunology & Institute of Immunology,Second Military Medical University;
- 英文论文关键词：CD11b ; Toll-like receptor ; IL-10 ; Src ; Colitis
- 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：R574.62
- 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：1
- 文件大小：379k
- 原文格式：D
- 会议级别：全国
摘要
Purpose:To investigate whether CD11 b and its signaling can control autoimmunity via IL-10 production.Methods:The colitis model was induced by DSS.Cytokines were assay by Q-PCR or ELISA.Signal transduction was detected by Westernblot.Results:CD11 b deficient(Itgam-/-) mice were more susceptible to DSS-induced colitis,with more TNF-α while less IL-10 production.CD11 b inhibited NF-κB while promoted AP-1 activation through activating Src,leading to decreased TNF-α while increased IL-10 production.Src interacted with and promoted c-Cbl-mediated degradation of the inhibitory subunit p85 of PI3 K.Importantly,Src inhibitor dasatinibaggravated DSS-induced colitis by decreasing IL-10 while increasing TNF-α in vivo.Therefore,CD11 b promotes IL-10 production by activating Src-Aktsignal pathway.Conclusion:An axis of CD11b-Src pathway is important in balancing homeostasis of TLR-induced pro-inflammatory and anti-inflammatory responses.
Purpose:To investigate whether CD11 b and its signaling can control autoimmunity via IL-10 production.Methods:The colitis model was induced by DSS.Cytokines were assay by Q-PCR or ELISA.Signal transduction was detected by Westernblot.Results:CD11 b deficient(Itgam-/-) mice were more susceptible to DSS-induced colitis,with more TNF-α while less IL-10 production.CD11 b inhibited NF-κB while promoted AP-1 activation through activating Src,leading to decreased TNF-α while increased IL-10 production.Src interacted with and promoted c-Cbl-mediated degradation of the inhibitory subunit p85 of PI3 K.Importantly,Src inhibitor dasatinibaggravated DSS-induced colitis by decreasing IL-10 while increasing TNF-α in vivo.Therefore,CD11 b promotes IL-10 production by activating Src-Aktsignal pathway.Conclusion:An axis of CD11b-Src pathway is important in balancing homeostasis of TLR-induced pro-inflammatory and anti-inflammatory responses.
Purpose:To investigate whether CD11 b and its signaling can control autoimmunity via IL-10 production.Methods:The colitis model was induced by DSS.Cytokines were assay by Q-PCR or ELISA.Signal transduction was detected by Westernblot.Results:CD11 b deficient(Itgam-/-) mice were more susceptible to DSS-induced colitis,with more TNF-α while less IL-10 production.CD11 b inhibited NF-κB while promoted AP-1 activation through activating Src,leading to decreased TNF-α while increased IL-10 production.Src interacted with and promoted c-Cbl-mediated degradation of the inhibitory subunit p85 of PI3 K.Importantly,Src inhibitor dasatinibaggravated DSS-induced colitis by decreasing IL-10 while increasing TNF-α in vivo.Therefore,CD11 b promotes IL-10 production by activating Src-Aktsignal pathway.Conclusion:An axis of CD11b-Src pathway is important in balancing homeostasis of TLR-induced pro-inflammatory and anti-inflammatory responses.
引文