Koide J, Takeuchi T, Hosono O, Takano M, Abe T
Department of Internal Medicine, Saitama Medical Center, Saitama Medical School, Japan.
Scand J Immunol. 1987 Oct;26(4):363-9. doi: 10.1111/j.1365-3083.1987.tb02268.x.
The present study was undertaken to determine the nature of the immunoregulatory T-cell defect after autologous mixed lymphocyte reaction (AMLR) activation in patients with systemic lupus erythematosus (SLE). Although AMLR was decreased in patients with SLE compared with normals, there was no difference in major proliferative cells (T4 cells and T4+JRA+ subset) in response to AMLR. Functional activity of AMLR-stimulated T4 subsets in patients with SLE and normals was examined in helper and suppressor/inducer assay, using pokeweed mitogen (PWM)-driven IgG synthesis. The T4+JRA- (helper) subset from SLE patients showed no greater activity than normals. However the T4+JRA+ (suppressor/inducer) subset from SLE patients showed decreased suppression induction compared with normals. This defect in the suppressor/inducer function was demonstrated even in patients with inactive SLR or in remission.
本研究旨在确定系统性红斑狼疮(SLE)患者自体混合淋巴细胞反应(AMLR)激活后免疫调节性T细胞缺陷的性质。尽管与正常人相比,SLE患者的AMLR降低,但对AMLR反应的主要增殖细胞(T4细胞和T4+JRA+亚群)并无差异。采用美洲商陆有丝分裂原(PWM)驱动的IgG合成,在辅助和抑制/诱导试验中检测了SLE患者和正常人中AMLR刺激的T4亚群的功能活性。SLE患者的T4+JRA-(辅助)亚群的活性并不高于正常人。然而,与正常人相比,SLE患者的T4+JRA+(抑制/诱导)亚群的抑制诱导作用降低。即使在无活动期SLE或缓解期患者中也证实了这种抑制/诱导功能缺陷。