Ruiz-Arguelles A, Alarcón-Segovia D, Llorente L, Del Giudice-Knipping J A
Arthritis Rheum. 1980 Sep;23(9):1004-9. doi: 10.1002/art.1780230907.
Eighty percent of 31 untreated patients with systemic lupus erythematosus (SLE) had abnormalities in their spontaneously expanded and/or Con-A-induced suppressor cell function, but the association of defects detected with both systems was only 68%. Loss of spontaneous suppression related positively to disease activity (r = 0.641) and the number of T gamma cells (r = 0.624) whereas Con-A-induced suppression correlated negatively with disease activity (r = -0.456) and the number of T gamma cells (r = 0.089). Incubation of mononuclear cells from SLE patients in antiribonucleoprotein IgG caused further loss of suppression in some, but not all, instances. The suppressor cell dysfunction found in SLE may result from diverse mechanisms, including a basic defect in the generation of suppressor cells and the abrogation of suppressor function by autoantibodies.
31例未经治疗的系统性红斑狼疮(SLE)患者中,80%的患者其自发扩增和/或刀豆蛋白A诱导的抑制细胞功能存在异常,但两种检测系统均检测到缺陷的关联度仅为68%。自发抑制功能的丧失与疾病活动度呈正相关(r = 0.641),与Tγ细胞数量呈正相关(r = 0.624),而刀豆蛋白A诱导的抑制作用与疾病活动度呈负相关(r = -0.456),与Tγ细胞数量呈负相关(r = 0.089)。在抗核糖核蛋白IgG中孵育SLE患者的单核细胞,在某些但并非所有情况下会导致抑制功能进一步丧失。SLE中发现的抑制细胞功能障碍可能由多种机制引起,包括抑制细胞生成的基本缺陷以及自身抗体对抑制功能的废除。