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肿瘤坏死因子与干扰素γ:对免疫调节及自身免疫性疾病遗传易感性的相关性

Tumor necrosis factor and interferon gamma: relevance for immune regulation and genetic predisposition to autoimmune disease.

作者信息

Jacob C O

机构信息

Department of Inflammation Biology and Immunology, Syntex Research, Palo Alto, CA 94303.

出版信息

Semin Immunol. 1992 Jun;4(3):147-54.

PMID:1627786
Abstract

The role of TNF-alpha and IFN-gamma in various models of autoimmune disease were analyzed. These include murine models of lupus, type 1 diabetes in NOD mice and the adjuvant arthritis model in rats. Rather than being involved mainly in the effector arm of the inflammatory process of autoimmune organ destruction, our data suggest a primary involvement of these cytokines in some of the basic mechanisms of the autoimmune process. Evidence has been presented that emphasizes the possibility of the involvement of TNF-alpha in the genetic predisposition to SLE. Based on the data presented, one should be cautious in extrapolating the effects of these cytokines in various in vitro systems to the in vivo situation.

摘要

分析了肿瘤坏死因子-α(TNF-α)和γ干扰素(IFN-γ)在各种自身免疫性疾病模型中的作用。这些模型包括狼疮的小鼠模型、非肥胖糖尿病(NOD)小鼠的1型糖尿病模型以及大鼠的佐剂性关节炎模型。我们的数据表明,这些细胞因子并非主要参与自身免疫性器官破坏炎症过程的效应环节,而是在自身免疫过程的一些基本机制中起主要作用。已有证据强调了TNF-α参与系统性红斑狼疮(SLE)遗传易感性的可能性。根据所呈现的数据,在将这些细胞因子在各种体外系统中的作用外推至体内情况时应谨慎。

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