Immunosuppressive exosomes from TGF-β1 gene-modified dendritic cells attenuate Th17-mediated inflammatory autoimmune disease by inducing regulatory T cells

摘要：

Dear Editor,Inflammatory bowel disease(IBD),including ulcerative colitis and Crohn”s disease,is generally believed to originate from the complicated interactions between genetic factors and commensal flora.This leads to the breakdown of innate immunity and the aberrant activation of the immune system,which is largely responsible for tissue damages in patients and animal models”1”.A new CD4+ T cell lineage,Th17,which predominantly produces IL-17,has been revealed recently to play a key role in the development of IBD.Studies in IL-17 receptor A(IL-17RA)-knockout mice have demonstrated that IL-17 is necessary for the development of IBD.Blockade of IL-17 signaling by an IL-17RA-IgG1 fusion protein significantly attenuated IBD”2”.

机标关键词：exosomes、T cells、autoimmune disease、development、IL-17、ulcerative colitis、innate immunity、genetic factors、fusion protein、immune system、animal models、interactions、IBD、breakdown、receptor、mice、CD4+、new、key

所属期刊栏目：22

分类号：Q2(细胞生物学)

在线出版日期：2012-06-28（万方平台首次上网日期，不代表论文的发表时间）

页码：607-610