Kaneoka H, Morito F, Yamaguchi M
Department of Internal Medicine, Saga Medical School, Japan.
J Clin Lab Immunol. 1989 Jan;28(1):15-26.
It has been widely accepted that murine monoclonal antibodies against the CD 3 antigen have mitogenic effects on human T cells which mimic antigen binding via the T cell receptors. We report that T cells from patients with active systemic lupus erythematosus cannot respond to anti Leu 4 antibody, an anti CD 3 murine monoclonal antibody of the subclass IgG1. It was observed that T cells from patients with the active disease expressed as much of the Leu 4 and OKT 3 epitopes as compared to high responders, and sera from active patients could not change the expression of the Leu 4 epitope. Similarly, the low responsiveness could not be attributed to suppressor T cells, poor production of IL 2 or less expression of the IL 2 receptor. The accessory nonrosetting mononuclear leucocytes from high responders could convert the low responsiveness of these patients to high, whereas the accessory cells from active patients failed to help the responses of T cells from high responders. Likewise, exogenous IL 1 and anti Leu 4 antibody bound to Sepharose beads independently or cooperatively failed to propagate T cells from low responders. We suggest that the low response to anti Leu 4 antibody as demonstrated in the T cells of patients with active SLE may be due in part to the impairment of the secondary signals, distinct from IL 1, between helping accessory cells and responding T cells, or to the dysfunction of intracellular transmission of stimulation, and may play significant roles in the pathogenesis of SLE.
人们普遍认为,针对CD 3抗原的鼠单克隆抗体对人T细胞具有促有丝分裂作用,这种作用通过T细胞受体模拟抗原结合。我们报告,活动性系统性红斑狼疮患者的T细胞不能对抗Leu 4抗体(一种IgG1亚类的抗CD 3鼠单克隆抗体)产生反应。观察到,与高反应者相比,活动性疾病患者的T细胞表达的Leu 4和OKT 3表位一样多,而且活动性患者的血清不能改变Leu 4表位的表达。同样,低反应性不能归因于抑制性T细胞、IL 2产生不足或IL 2受体表达减少。高反应者的非凝集单核白细胞可将这些患者的低反应性转变为高反应性,而活动性患者的辅助细胞不能促进高反应者T细胞的反应。同样,与琼脂糖珠结合的外源性IL 1和抗Leu 4抗体单独或协同作用均不能使低反应者的T细胞增殖。我们认为,活动性SLE患者T细胞中所显示的对抗Leu 4抗体的低反应性可能部分归因于辅助性细胞与反应性T细胞之间不同于IL 1的第二信号受损,或细胞内刺激传递功能障碍,并且可能在SLE的发病机制中起重要作用。