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白细胞介素-17及其家族成员在关节炎发病机制中的作用。

The role of IL-17 and family members in the pathogenesis of arthritis.

作者信息

Lubberts Erik

机构信息

University Medical Center Nijmegen, Geert Grooteplein Zuid 26-28, 6500 HB, Nijmegen, The Netherlands.

出版信息

Curr Opin Investig Drugs. 2003 May;4(5):572-7.

Abstract

Interleukin (IL)-17 is a T-cell-derived cytokine that is expressed in the synovium of patients with arthritis. IL-17 contributes to the pathogenesis of arthritis, and demonstrates additive or even synergistic effects with IL-1 and tumor necrosis factor (TNF) in inducing joint pathology. It is a potent inducer of receptor activator of nuclear factor-kappa B. IL-17 also has the capacity to induce joint destruction in an IL-1-independent manner. The discovery of IL-17 family members may further elucidate the role of this cytokine family in arthritis pathology, with IL-17F a promising candidate. Anti-IL-17 cytokine therapy may be an interesting new antirheumatic approach to the prevention of joint destruction, in addition to anti-TNF and anti-IL-1 therapy.

摘要

白细胞介素(IL)-17是一种由T细胞产生的细胞因子,在关节炎患者的滑膜中表达。IL-17参与关节炎的发病机制,并且在诱导关节病变方面与IL-1和肿瘤坏死因子(TNF)具有相加甚至协同作用。它是核因子-κB受体激活剂的强效诱导剂。IL-17还能够以不依赖IL-1的方式诱导关节破坏。IL-17家族成员的发现可能会进一步阐明该细胞因子家族在关节炎病理中的作用,其中IL-17F是一个有前景的候选者。除了抗TNF和抗IL-1治疗之外,抗IL-17细胞因子治疗可能是一种预防关节破坏的有趣的新型抗风湿方法。

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