Interleukin‐19 ameliorates experimental autoimmune encephalitis
Interleukin‐19 ameliorates experimental autoimmune encephalitis
复制标题
Interleukin-19 可改善实验性自身免疫性脑炎
DOI：
10.1111/cen3.12642
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发表时间：
2021
影响因子：
--
通讯作者：
Suzumura Akio
中科院分区：
文献类型：
--
作者：
Takeuchi Hideyuki;Horiuchi Hiroshi;Parajuli Bijay;Komiya Hiroyasu;Tanaka Fumiaki;Suzumura Akio
IL-19抑制小胶质细胞/巨噬细胞抗原提呈、T辅助17细胞扩张和中枢神经系统随后的炎症，从而改善实验性自身免疫性脑脊髓炎。关键词：抗原提呈；巨噬细胞；小胶质细胞；多发性硬化；T辅助17细胞抗原提呈巨噬细胞小胶质细胞多发性硬化症T辅助17细胞148 149 2 09/02/21 20210801 NES 210801白细胞介素19作为负反馈调节因子以自分泌/旁分泌的方式限制巨噬细胞和小胶质细胞的促炎反应。这些数据表明，IL-19通过抑制中枢神经系统小胶质细胞/巨噬细胞抗原提呈、Th17细胞扩张和随后的炎症，在抑制MS发病中发挥关键作用。[摘自文章]《临床与实验神经免疫学》版权归Wiley-Blackwell所有，未经版权所有者明确书面许可，不得将其内容复制或通过电子邮件发送到多个站点或发布到列表服务器。但是，用户可以打印、下载或通过电子邮件发送文章供个人使用。这篇摘要可以删节。对复制品的准确性不作任何保证。用户应参考该材料的原始出版版本，以获取完整摘要。版权适用于所有摘要。
Interleukin-19 suppresses microglia/macrophage antigen presentation, T helper 17 cell expansion and subsequent inflammation in the central nervous system, resulting in improvement in experimental autoimmune encephalomyelitis. Keywords: antigen presentation; macrophage; microglia; multiple sclerosis; T helper 17 cell EN antigen presentation macrophage microglia multiple sclerosis T helper 17 cell 148 149 2 09/02/21 20210801 NES 210801 Interleukin-19 serves as a negative feedback regulator to limit the pro-inflammatory response of macrophages and microglia in autocrine/paracrine manners. These data showed that IL-19 plays a pivotal role in the suppression of MS pathogenesis by inhibiting microglia/macrophage antigen presentation, Th17 cell expansion and subsequent inflammation in the CNS.[Extracted from the article]Copyright of Clinical & Experimental Neuroimmunology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. Copyright applies to all Abstracts.