Oncogenic inflammation and autoimmune disease

被引:22
作者
Eisenlohr, Laurence C.
Rothstein, Jay L.
机构
[1] Thomas Jefferson Univ, Kimmel Canc Ctr, HNS, Dept Microbiol & Immunol, Philadelphia, PA 19107 USA
[2] Thomas Jefferson Univ, Kimmel Canc Ctr, HNS, Dept Otolaryngol, Philadelphia, PA 19107 USA
关键词
cytokines; fusion protein; inflammation; oncogene; T cells; tyrosine kinases;
D O I
10.1016/j.autrev.2006.04.002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Many models exist to explain the induction and perpetuation of autoimmune diseases. Despite their validation in a variety of animal models, the basis for autoimmune disease in humans remains unknown. Here, we propose that an important aspect of autoimmune disease is the active participation of the target organ due to endogenously produced co-stimulatory factors that cause prolonged antigen presentation and lymphocyte activation. Evidence suggests that a major source of such endogenous signaling comes from newly transformed cells within the target organ that produce pro-inflammatory factors. (c) 2006 Published by Elsevier B.V.
引用
收藏
页码:107 / 114
页数:8
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