Dinarello C A
Department of Medicine, Tufts University, Boston, MA 02111.
Semin Immunol. 1992 Jun;4(3):133-45.
Autoimmune diseases have been studied from the perspective of an abnormal immune response in genetically vulnerable hosts. Although the immune response is responsible for the initiation of autoimmune diseases, the effectors of the disease process likely involves cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF). These polypeptides induce a wide variety of inflammatory events which contribute to the destruction of tissue and tissue remodeling in several autoimmune diseases. Blocking IL-1 with its naturally occurring receptor antagonist, the IL-1 receptor antagonist reduces the severity of disease in animal models of inflammation and autoimmune processes. Clinical studies with the IL-1 receptor antagonist will define the role for this cytokine in the pathogenesis of autoimmune diseases such as arthritis, inflammatory bowel disease, type I diabetes and vasculitis.
自身免疫性疾病已从基因易感性宿主异常免疫反应的角度进行了研究。虽然免疫反应是自身免疫性疾病起始的原因，但疾病进程的效应器可能涉及细胞因子，如白细胞介素-1（IL-1）和肿瘤坏死因子（TNF）。这些多肽会引发多种炎症事件，在几种自身免疫性疾病中导致组织破坏和组织重塑。用其天然存在的受体拮抗剂阻断IL-1，即IL-1受体拮抗剂，可减轻炎症和自身免疫过程动物模型中的疾病严重程度。使用IL-1受体拮抗剂的临床研究将确定这种细胞因子在关节炎、炎症性肠病、I型糖尿病和血管炎等自身免疫性疾病发病机制中的作用。
