Dinarello C A
Tufts University, Boston, Massachusetts.
Curr Opin Immunol. 1991 Dec;3(6):941-8. doi: 10.1016/s0952-7915(05)80018-4.
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.
引发自身免疫性疾病的事件性质各异。白细胞介素 -1 和肿瘤坏死因子并不会引发自身免疫性疾病，而是充当效应分子。它们诱导类花生酸和一氧化氮的合成，刺激胶原酶和胶原蛋白的合成，并触发其他细胞因子的基因，即白细胞介素 -2、白细胞介素 -6 和白细胞介素 -8。用受体拮抗剂阻断白细胞介素 -1 以及用可溶性受体阻断肿瘤坏死因子的能力，为研究人员提供了特定工具，用以测试这两种细胞因子在自身免疫性疾病病理过程中的作用。
