Imai F, Suzuki T, Ishibashi T, Tanaka M, Akiyama Y, Dohi Y
Second Department of Internal Medicine, Saitama Medical School, Japan.
J Rheumatol. 1994 Apr;21(4):612-5.
We investigated the in vitro immunomodulatory effects of sulfasalazine on B cells in rheumatoid arthritis (RA).
Reversed hemolytic plaque assay and 3H-thymidine incorporation were measured.
B cells from patients with RA showed hyperactivity to stimulation by Staphylococcus aureus Cowan I. Sulfasalazine significantly inhibited this B cell hyperactivity in a dose dependent manner. The kinetic study and a decrease in 3H-thymidine incorporation on Day 3 indicate that sulfasalazine inhibited the early phase (0-48 h) of B cell proliferation in these patients. Sulfapyridine also inhibited B cell hyperactivity in these patients, but 5-aminosalicylic acid and N-acetylsulfapyridin had no significant effect.
Sulfasalazine exhibited a direct immunosuppressive effect on B cell hyperactivity in patients with RA, which may be responsible for its therapeutic effectiveness in this disorder.
我们研究了柳氮磺胺吡啶对类风湿关节炎(RA)患者B细胞的体外免疫调节作用。
采用反向溶血空斑试验和³H-胸腺嘧啶核苷掺入法进行检测。
RA患者的B细胞对金黄色葡萄球菌Cowan I刺激表现出高反应性。柳氮磺胺吡啶以剂量依赖方式显著抑制这种B细胞高反应性。动力学研究以及第3天³H-胸腺嘧啶核苷掺入量的减少表明,柳氮磺胺吡啶抑制了这些患者B细胞增殖的早期阶段(0 - 48小时)。磺胺吡啶也抑制这些患者的B细胞高反应性,但5-氨基水杨酸和N-乙酰磺胺吡啶无显著作用。
柳氮磺胺吡啶对RA患者的B细胞高反应性表现出直接免疫抑制作用,这可能是其对该疾病具有治疗效果的原因。