Regulation of autoimmune inflammation by pro-inflammatory cytokines.

Regulation of autoimmune inflammation by pro-inflammatory cytokines.
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DOI:
10.1016/j.imlet.2008.07.008
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发表时间:
2008-10-30
期刊:
影响因子:
4.4
通讯作者:
Moudgil, Kamal D.
Moudgil, Kamal D.
中科院分区:
医学3区
文献类型:
--
作者:
Kim, Eugene Y.;Moudgil, Kamal D.

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促炎细胞因子在自身免疫性关节炎和许多其他由失调的自我导向免疫应答引起的疾病的起始和传播中起关键作用。这些细胞因子在多个水平上影响炎症的细胞、免疫和生化介质之间的相互作用。这些细胞因子的促炎活性的调节通常被认为是由抗炎和免疫抑制细胞因子如IL-4、IL-10或TGF-β介导的。然而,在糖尿病、多发性硬化、葡萄膜炎和狼疮的动物模型中进行的研究中,越来越多的证据支持促炎细胞因子本身的调节属性。我们最近的研究结果表明,促炎细胞因子TNF-α和IFN-γ可以抑制大鼠的关节炎炎症,并且还有助于抵抗关节炎。这些结果不仅在充分理解自身免疫性关节炎的发病机制方面,而且在预测促炎细胞因子的体内中和的全部后果(包括用于治疗目的的中和)方面具有极其重要的意义。
The pro-inflammatory cytokines play a critical role in the initiation and propagation of autoimmune arthritis and many other disorders resulting from a dysregulated self-directed immune response. These cytokines influence the interplay among the cellular, immunological and biochemical mediators of inflammation at multiple levels. Regulation of the pro-inflammatory activity of these cytokines is generally perceived to be mediated by the anti-inflammatory and immunosuppressive cytokines such as IL-4, IL-10, or TGF-β. However, increasing evidence is accumulating in support of the regulatory attributes of the pro-inflammatory cytokines themselves, in studies conducted in animal models of diabetes, multiple sclerosis, uveitis, and lupus. The results of our recent studies have shown that the pro-inflammatory cytokines, TNF-α and IFN-γ, can suppress arthritic inflammation in rats, and also contribute to resistance against arthritis. These results are of paramount significance not only in fully understanding the pathogenesis of autoimmune arthritis, but also in anticipating the full ramifications of the in vivo neutralization of the pro-inflammatory cytokines, including that for therapeutic purposes.
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