Keystone E C, Shore A, Miller R G, Tan P, Poplonski L, Leary P, Albert S
J Rheumatol Suppl. 1983 Dec;11:85-92.
We have previously demonstrated defective antigen specific T-suppressor (Ts) cell function in the peripheral blood lymphocytes (PBL) from patients with rheumatoid arthritis (RA). Our study was designed to delineate whether diminished Ts activity is due to impaired interleukin (IL) dependent clonal expansion of Ts cells or to prior in vivo activation. Patients with recent onset of RA, or a disease flare, exhibited enhanced IL generation (IL-1 and /or IL-2). Increased proportions of active E-rosettes, elevated spontaneous production of IgM, and total immunoglobulin in mitogen free cultures were consistent with the concept of prior lymphocyte activation in vivo. Our results do not support defective clonal expansion of Ts cells as the basis of deficient IL generation, but do support the concept of in vivo activation of PBM cells in some patients with RA.
我们先前已证明，类风湿性关节炎（RA）患者外周血淋巴细胞（PBL）中存在抗原特异性T抑制（Ts）细胞功能缺陷。我们的研究旨在确定Ts活性降低是由于Ts细胞依赖白细胞介素（IL）的克隆扩增受损，还是由于先前的体内激活所致。近期发病或病情复发的RA患者表现出IL生成增强（IL-1和/或IL-2）。活性E花环比例增加、无丝裂原培养中IgM和总免疫球蛋白的自发产生升高，与体内先前淋巴细胞激活的概念一致。我们的结果不支持Ts细胞克隆扩增缺陷是IL生成不足的基础这一观点，但支持一些RA患者体内PBM细胞被激活的概念。
