Maini R N, Elliott M, Brennan F M, Williams R O, Feldmann M
Kennedy Institute of Rheumatology, London, UK.
APMIS. 1997 Apr;105(4):257-63. doi: 10.1111/j.1699-0463.1997.tb00567.x.
The role of the immune response in rheumatoid arthritis (RA) is a subject of debate, although it is widely believed to be a T-cell-driven disease. Progress is being hindered by lack of convincing evidence of a defined specific antigen initiating or perpetuating the response. Clinical trials using monoclonal antibodies directed against T-cell surface molecules such as CD4. CD5, and CD7 have thus far not provided evidence of efficacy. The negative data may reflect inadequate dosing or could suggest that indiscriminate depletion of T cells is insufficient by itself as a therapeutic strategy. Blocking proinflammatory cytokines (e.g. TNF alpha, IL-1) or augmenting anti-inflammatory cytokines (e.g. IL-10) offers an alternative approach to therapy. Clinical trials using monoclonal anti-TNF alpha have been particularly successful in controlling inflammation and markedly reducing acute phase proteins and cellular ingress. However, because disease invariably relapses, repeated therapy is necessary. Preliminary experience suggests that this is possible. Anti-TNF therapy for RA has defined a molecular target and new approach for treating immuno-inflammatory disorders.
免疫反应在类风湿性关节炎（RA）中的作用是一个有争议的话题，尽管人们普遍认为它是一种由T细胞驱动的疾病。由于缺乏确凿证据证明存在引发或维持该反应的特定抗原，研究进展受到阻碍。迄今为止，使用针对T细胞表面分子（如CD4、CD5和CD7）的单克隆抗体进行的临床试验尚未提供疗效证据。这些阴性数据可能反映出剂量不足，或者可能表明不加区分地消耗T细胞本身作为一种治疗策略是不够的。阻断促炎细胞因子（如肿瘤坏死因子α、白细胞介素-1）或增强抗炎细胞因子（如白细胞介素-10）提供了一种替代治疗方法。使用单克隆抗肿瘤坏死因子α的临床试验在控制炎症以及显著降低急性期蛋白和细胞浸润方面特别成功。然而，由于疾病总是会复发，因此需要重复治疗。初步经验表明这是可行的。针对类风湿性关节炎的抗TNF治疗确定了一个分子靶点以及治疗免疫炎症性疾病的新方法。
