Nakaike S, Tanaka C, Tomita N, Umemoto M, Otomo S, Aihara H
Jpn J Pharmacol. 1983 Oct;33(5):983-90. doi: 10.1254/jjp.33.983.
Effects of D-penicillamine-L-cysteine disulfide (P-C) on some immunological parameters were examined in normal and immunity-impaired mice and rats. P-C enhanced the DNA synthesis in concanavalin A-stimulated mouse spleen cell cultures in vitro. In vivo, administration of P-C produced either enhancement or depression of plaque forming cell (PFC) response and delayed type hypersensitivity (DTH) to sheep red blood cells (SRBC) in low responder mice to SRBC, depending on the dose of P-C. P-C restored the impaired PFC response in hydrocortisone-pretreated mice. The enhancing effect of P-C was not shown in high responder mice to SRBC, but an inhibiting effect was observed. P-C inhibited the suppressor cell induction on PFC response in mice immunized with a supraoptimum dose of antigen. In adjuvant arthritic rats, P-C induced severe arthritis by eliminating the suppressor cells regulating this disease process. The relevance of these findings and mode of action of D-penicillamine in rheumatoid arthritis is discussed.
在正常及免疫受损的小鼠和大鼠中研究了D-青霉胺-L-半胱氨酸二硫化物（P-C）对一些免疫学参数的影响。P-C增强了体外伴刀豆球蛋白A刺激的小鼠脾细胞培养物中的DNA合成。在体内，给予P-C对低反应性小鼠体内针对绵羊红细胞（SRBC）的空斑形成细胞（PFC）反应和迟发型超敏反应（DTH）产生增强或抑制作用，这取决于P-C的剂量。P-C恢复了氢化可的松预处理小鼠中受损的PFC反应。P-C对高反应性小鼠针对SRBC未显示出增强作用，但观察到有抑制作用。P-C抑制了用超最佳剂量抗原免疫的小鼠中PFC反应的抑制细胞诱导。在佐剂性关节炎大鼠中，P-C通过消除调节该疾病过程的抑制细胞而诱发严重关节炎。讨论了这些发现与D-青霉胺在类风湿性关节炎中的作用方式的相关性。
