肿瘤坏死因子-α在佐剂诱导性关节炎中的矛盾效应。
Paradoxical effects of tumour necrosis factor-alpha in adjuvant-induced arthritis.
作者信息
Williams Richard O
出版信息
Arthritis Res Ther. 2008;10(3):113. doi: 10.1186/ar2430. Epub 2008 Jun 6.
Abstract
Anti-tumour necrosis factor (TNF)alpha therapy is highly effective in rheumatoid arthritis and it is surprising, therefore, that a recent study showed that intraperitoneal administration of recombinant TNFalpha reduced the severity of adjuvant-induced arthritis and decreased IFNgamma expression in cultured draining lymph node cells. Furthermore, in untreated arthritic rats, maximal TNFalpha expression in draining lymph node cells coincided with spontaneous disease remission, suggesting a role for endogenous TNFalpha in recovery from arthritis. If confirmed in further studies, these findings suggest that, in addition to its well-established pro-inflammatory properties, TNFalpha may also play a disease-limiting role in this model of rheumatoid arthritis by suppressing effector T cell responses.
摘要
抗肿瘤坏死因子（TNF）α疗法在类风湿性关节炎中具有高度疗效，因此，一项近期研究显示腹腔注射重组TNFα可减轻佐剂诱导性关节炎的严重程度，并降低培养的引流淋巴结细胞中的IFNγ表达，这令人惊讶。此外，在未经治疗的关节炎大鼠中，引流淋巴结细胞中TNFα的最大表达与自发性疾病缓解同时出现，提示内源性TNFα在关节炎恢复中发挥作用。如果在进一步研究中得到证实，这些发现表明，除了其已确立的促炎特性外，TNFα在这种类风湿性关节炎模型中可能还通过抑制效应T细胞反应发挥疾病限制作用。
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