Feldmann M
Kennedy Institute of Rheumatology, Sunley Division, London, UK.
Int Arch Allergy Immunol. 1996 Dec;111(4):362-5. doi: 10.1159/000237393.
The rationale for anti-tumour necrosis factor-alpha (anti-TNFalpha) therapy in rheumatoid arthritis (RA) is based on experiments on cultures of human rheumatoidjoint tissue, supported by experiments in animal models, all of which demonstrated that anti-TNFalpha antibody had profound effects on the disease activity. Clinical trials have substantiated this concept, and we have used the serum samples from the clinical trials, as well as biopsies to study the changes occurring during anti-TNFalpha therapy as clues to the pathogenesis of RA. The major effects of anti-TNFalpha therapy are in downregulating cytokine activity, and in reducing leucocyte trafficking to the joints.
肿瘤坏死因子-α（抗TNFα）疗法用于类风湿关节炎（RA）的理论依据基于对人类类风湿关节组织培养的实验，并得到动物模型实验的支持，所有这些实验均表明抗TNFα抗体对疾病活动有深远影响。临床试验证实了这一概念，并且我们利用临床试验的血清样本以及活检组织来研究抗TNFα治疗期间发生的变化，以此作为RA发病机制的线索。抗TNFα治疗的主要作用是下调细胞因子活性，并减少白细胞向关节的迁移。
