期刊
CLINICAL IMMUNOLOGY
卷 100, 期 2, 页码 198-207出版社
ACADEMIC PRESS INC
DOI: 10.1006/clim.2001.5059
关键词
autoimmunity; diabetes; TNF-alpha receptor; T cells; LIGHT; HVEM
类别
资金
- NIDDK NIH HHS [DK 57644-01] Funding Source: Medline
Insulin-dependent diabetes mellitus results from T-cell-mediated destruction of pancreatic islet beta cells. Both CD4 and CD8 T cells have been shown to be independently capable of beta cell destruction. However, the mechanism of beta cell destruction has remained elusive. It has previously been shown that the absence of TNF-alpha receptor 1 (p55) on the islets protected islets from CD4 T-cell-mediated destruction as long as the T cells did not have access to wild-type islets in vivo. Wild-type and TNF-alpha receptor 1 (p55) deficient islets induce similar levels of proliferation of BDC2.5 T cells. In this study, we demonstrate that islet TNF-alpha receptor I (p55) influences the expression of LIGHT (TNFSF-14), a TNF family member with both cytolytic and costimulatory properties, on BDC2.5 T cells and the expression of its receptor HVEM (TNFRSF-14) by islets, indicating a role for LIGHT-HVEM interactions in autoimmune diabetes. (C) 2001 Academic Press.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据