RKIP mediates autoimmune inflammation by positively regulating IL-17R signaling
文献类型：期刊论文
| 作者 | Lin, Wenlong4,5; Wang, Ning5; Su, Fasheng5; Shou, Jianan5; Liu, Huan5; Ma, Chunmei5; Wang, Xiaojian5; Wang, Kai4; Zhou, Kangxing3; Jiang, Yu2 |
| 刊名 | EMBO REPORTS
 |
| 出版日期 | 2018 |
| 卷号 | 19期号:6页码:UNSP e44951 |
| 关键词 | Act1 EAE IL-17 RKIP |
| ISSN号 | 1469-221X |
| DOI | 10.15252/embr.201744951 |
| 文献子类 | Article |
| 英文摘要 | Th17 cells contribute to the development of autoimmune diseases by secreting interleukin-17 (IL-17), which activates its receptor (IL-17R) that is expressed on epithelial cells, macrophages, microglia, and resident neuroectodermal cells. However, the mechanisms through which IL-17R-mediated signaling contributes to the development of autoimmune disease have not been completely elucidated. Here, we demonstrate that Raf-1 kinase inhibitor protein (RKIP) deficiency in mice ameliorates the symptoms of experimental autoimmune encephalomyelitis (EAE). Adoptive T-cell-transfer experiments demonstrate that RKIP plays a predominant role in Th17-mediated, but not in Th1-mediated immune responses. RKIP deficiency has no effect on Th17-cell differentiation ex vivo, nor does it affect Th17-cell differentiation in EAE mice. However, RKIP significantly promotes IL-17R-induced proinflammatory cytokine and chemokine production. Mechanistically, RKIP directly interacts with IL-17RA and Act1 to promote the formation of an IL-17R-Act1 complex, resulting in enhanced MAPK- and P65-mediated NF-B activation and downstream cytokine production. Together, these findings indicate that RKIP functions as an essential modulator of the IL-17R-Act1 axis in IL-17R signaling, which promotes IL-17-induced inflammation and autoimmune neuroinflammation. |
| 学科主题 | Biochemistry & Molecular Biology ; Cell Biology |
| WOS关键词 | CENTRAL-NERVOUS-SYSTEM ; NF-KAPPA-B ; INTERLEUKIN-17 FAMILY-MEMBERS ; MULTIPLE-SCLEROSIS ; KINASE-ACTIVITY ; PROTEIN RKIP ; CANCER-CELLS ; ACTIVATION ; ACT1 ; METASTASIS |
| 语种 | 英语 |
| WOS记录号 | WOS:000434352400003 |
| 出版者 | WILEY |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/511]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所 |
| 作者单位 | 1.Shanghai Jiao Tong Univ, Chinese Acad Sci, Shanghai Inst Biol Sci, Key Lab Stem Cell Biol,Inst Hlth Sci,Sch Med, Shanghai, Peoples R China, 2.Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Clin Lab Med, Hangzhou, Zhejiang, Peoples R China; 3.Nanjing Univ, Affiliated Drum Tower Hosp, Med Sch, Dept Rheumatol & Immunol, Nanjing, Jiangsu, Peoples R China; 4.Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Resp Med, Hangzhou, Zhejiang, Peoples R China; 5.Zhejiang Univ, Sch Med, Inst Immunol, Hangzhou, Zhejiang, Peoples R China; |
| 推荐引用方式 GB/T 7714 | Lin, Wenlong,Wang, Ning,Su, Fasheng,et al. RKIP mediates autoimmune inflammation by positively regulating IL-17R signaling[J]. EMBO REPORTS,2018,19(6):UNSP e44951. |
| APA | Lin, Wenlong.,Wang, Ning.,Su, Fasheng.,Shou, Jianan.,Liu, Huan.,...&,.(2018).RKIP mediates autoimmune inflammation by positively regulating IL-17R signaling.EMBO REPORTS,19(6),UNSP e44951. |
| MLA | Lin, Wenlong,et al."RKIP mediates autoimmune inflammation by positively regulating IL-17R signaling".EMBO REPORTS 19.6(2018):UNSP e44951. |
入库方式： OAI收割
来源：上海营养与健康研究所
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