Isaacs J D
Musculoskeletal Research Group and Wilson Horne Immunotherapy Centre, Institute of Cellular Medicine, Newcastle University, Newcastle-upon-Tyne, UK.
Rheumatology (Oxford). 2008 Oct;47(10):1461-8. doi: 10.1093/rheumatology/ken163. Epub 2008 May 25.
Accumulating evidence suggests that RA is a T-cell-mediated autoimmune disease. Early attempts at disease modulation using strategies such as CD4 mAbs were severely hampered by a lack of biomarkers of autoreactivity. Recently, however, co-stimulation blockade has emerged as an effective treatment for RA. Alongside a greatly improved mechanistic understanding of immune regulation, this has rekindled hopes for authentic and robust immune programming. The final pieces of the jigsaw are not yet in place for RA but, in other disciplines, emerging treatment paradigms such as non-mitogenic anti-CD3 mAbs, autoantigenic peptides and even cellular therapies are providing hope for a future in which immunopathology can be specifically and vigorously curtailed.
越来越多的证据表明类风湿性关节炎是一种由T细胞介导的自身免疫性疾病。早期尝试使用如CD4单克隆抗体等策略进行疾病调节时,由于缺乏自身反应性生物标志物而受到严重阻碍。然而,最近共刺激阻断已成为类风湿性关节炎的一种有效治疗方法。随着对免疫调节机制的理解有了极大的改进,这重新燃起了实现真实且强大的免疫编程的希望。类风湿性关节炎的拼图最后几块尚未就位,但在其他学科中,诸如非促有丝分裂抗CD3单克隆抗体、自身抗原肽甚至细胞疗法等新兴治疗模式,为未来能够特异性且有力地减少免疫病理学问题带来了希望。