INFLAMMATORY CYTOKINES - INTERLEUKIN-1 AND TUMOR-NECROSIS-FACTOR AS EFFECTOR MOLECULES IN AUTOIMMUNE-DISEASES

被引:159
作者
DINARELLO, CA [1 ]
机构
[1] NEW ENGLAND MED CTR HOSP,BOSTON,MA 02111
关键词
D O I
10.1016/S0952-7915(05)80018-4
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The nature of the events that precipitate autoimmune diseases varies. Interleukin-1 and tumor necrosis factor do not precipitate autoimmune diseases but rather act as effector molecules. They induce eicosanoid and nitric oxide synthesis, stimulate collagenases and collagen synthesis, and trigger the genes for other cytokines, namely interleukin-2, interleukin-6 and interleukin-8. The ability to block interleukin-1 with the receptor antagonist, and tumor necrosis factor with soluble receptors, has given investigators specific tools to test the role of these two cytokines in the pathological processes of autoimmune disease.
引用
收藏
页码:941 / 948
页数:8
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