Pelegrí C, Morante M P, Castellote C, Franch A, Castell M
Unit of Physiology, Faculty of Pharmacy, University of Barcelona, Spain.
Clin Exp Immunol. 1996 Feb;103(2):273-8. doi: 10.1046/j.1365-2249.1996.d01-624.x.
Some experimental arthritic diseases can be prevented by treatment with anti-CD4 MoAbs. Trials with ongoing disease have not been successful so far. The aim of this study was to ascertain whether W3/25 could reverse adjuvant arthritis (AA), when beginning treatment on day 14, i.e. when the disease was established. Moreover, one group of animals treated with the anti-CD4 MoAb received OX8 MoAb at the same time, thus depleting CD8+ cells from circulation. During treatment with W3/25, a strong amelioration of inflammatory signals were observed, as assessed by means of paw volume increase and arthritic score. However, when treatment stopped, a rebound to arthritis signals occurred. The parallel depletion of CD8+ cells did not modify these effects, thus the combined treatment W3/25 + OX8 gave the same amelioration as treatment with W3/25 alone. These findings indicate that CD4+ cells play an important role in perpetuating rat AA. Moreover, CD8+ cells do not seem to have a regulatory role int he CD4+ cells responsible for the inflammatory response.
一些实验性关节炎疾病可以通过抗CD4单克隆抗体治疗来预防。到目前为止，针对已患疾病的试验尚未成功。本研究的目的是确定在第14天开始治疗（即疾病已确立时）时，W3/25是否能逆转佐剂性关节炎（AA）。此外，一组用抗CD4单克隆抗体治疗的动物同时接受OX8单克隆抗体，从而使循环中的CD8+细胞耗竭。在用W3/25治疗期间，通过爪体积增加和关节炎评分评估，观察到炎症信号有明显改善。然而，当治疗停止时，关节炎信号出现反弹。CD8+细胞的平行耗竭并未改变这些效应，因此W3/25 + OX8联合治疗与单独使用W3/25治疗的改善效果相同。这些发现表明，CD4+细胞在大鼠AA的持续发展中起重要作用。此外，CD8+细胞似乎在负责炎症反应的CD4+细胞中没有调节作用。
