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用抗gp39(CD40的配体)抗体预防胶原诱导的关节炎。

Prevention of collagen-induced arthritis with an antibody to gp39, the ligand for CD40.

作者信息

Durie F H, Fava R A, Foy T M, Aruffo A, Ledbetter J A, Noelle R J

机构信息

Department of Microbiology, Dartmouth Medical School, Lebanon, NH 03756.

出版信息

Science. 1993 Sep 3;261(5126):1328-30. doi: 10.1126/science.7689748.

Abstract

The ligand for the CD40 antigen is a 39-kilodalton protein, gp39, expressed on the surface of activated CD4+ T cells and is essential for thymus-dependent humoral immunity. The role of gp39-CD40 interactions in autoimmune disease was investigated in vivo with the use of an antibody that blocks their interactions (anti-gp39). Arthritis induced in mice by immunization with type II collagen was inhibited by anti-gp39. Anti-gp39 blocked the development of joint inflammation, serum antibody titers to collagen, the infiltration of inflammatory cells into the subsynovial tissue, and the erosion of cartilage and bone. Thus, interference with gp39-CD40 interactions may have therapeutic potential in the treatment of autoimmune disease.

摘要

CD40抗原的配体是一种39千道尔顿的蛋白质,即gp39,它表达于活化的CD4+T细胞表面,对胸腺依赖性体液免疫至关重要。利用一种能阻断它们相互作用的抗体(抗gp39)在体内研究了gp39-CD40相互作用在自身免疫性疾病中的作用。用II型胶原免疫小鼠诱导的关节炎被抗gp39抑制。抗gp39可阻断关节炎症的发展、针对胶原的血清抗体滴度、炎症细胞向滑膜下组织的浸润以及软骨和骨的侵蚀。因此,干扰gp39-CD40相互作用可能在自身免疫性疾病的治疗中具有治疗潜力。

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