Lewins E G, Clancy R L, Cripps A W, Glass J S, Major G A
J Rheumatol. 1985 Aug;12(4):685-91.
We assessed the immunoglobulin secretory capacity of circulating B lymphocytes in 9 patients with classical rheumatoid arthritis (RA) before and after treatment with D-penicillamine. Peripheral blood lymphocytes (PBL) from patients with RA spontaneously synthesized more IgG and IgA than normals. The secretory rate of rheumatoid PBL could not be induced by the polyclonal activator, pokeweed mitogen (PWM). The presence of D-penicillamine in cultures significantly suppressed PWM stimulated immunoglobulin synthesis of control PBL but did not inhibit synthesis of mitogen stimulated RA PBL. After D-penicillamine therapy for 3 months immunoglobulin synthesis by PBL from patients with RA was reduced with or without PWM. The T mu:T gamma ratio was also decreased after therapy. These results support the hypothesis that D-penicillamine selectively impairs helper T cells in vivo, preventing the T dependent expansion and activation of B cells characteristic of RA.
我们评估了9例典型类风湿关节炎(RA)患者在青霉胺治疗前后循环B淋巴细胞的免疫球蛋白分泌能力。类风湿关节炎患者的外周血淋巴细胞(PBL)自发合成的IgG和IgA比正常人更多。类风湿PBL的分泌率不能被多克隆激活剂商陆丝裂原(PWM)诱导。培养物中存在青霉胺可显著抑制PWM刺激的对照PBL的免疫球蛋白合成,但不抑制丝裂原刺激的类风湿关节炎PBL的合成。在青霉胺治疗3个月后,无论有无PWM,类风湿关节炎患者PBL的免疫球蛋白合成均减少。治疗后Tμ:Tγ比值也降低。这些结果支持了这样的假设,即青霉胺在体内选择性损害辅助性T细胞,阻止类风湿关节炎特有的T细胞依赖性B细胞扩增和激活。