Indiveri F, Scudeletti M, Pierri I, Traverso A, Cerri C, Ferrone S
Cell Immunol. 1986 Jan;97(1):197-203. doi: 10.1016/0008-8749(86)90389-8.
Analysis of T cells from patients with systemic lupus erythematosus (SLE) and with rheumatoid arthritis (RA) identified a deficit in the induction of HLA Class II antigens by PHA although the proliferative response was normal and in the [3H]thymidine incorporation in autologous mixed lymphocyte reactions (MLR) with PHA-T cells as stimulators. In RA these abnormalities were more marked in patients with active disease than in those in clinical remission. The deficit of autologous MLR with PHA-T cells was more marked than that of autologous MLR with non-T cells and of allogeneic MLR. Serum from patients with SLE and with RA did not display any detectable inhibitory activity on the induction of HLA Class II antigens by PHA, on the proliferative response of lymphocytes to PHA, on autologous MLR with PHA-T cells and with non-T cells as stimulators and on allogeneic MLR. These results suggest that the abnormalities we have identified reflect an intrinsic defect of T cells.
对系统性红斑狼疮（SLE）患者和类风湿性关节炎（RA）患者的T细胞分析发现，尽管增殖反应正常且在以PHA - T细胞作为刺激物的自体混合淋巴细胞反应（MLR）中[3H]胸苷掺入正常，但PHA诱导HLA - II类抗原存在缺陷。在RA中，这些异常在疾病活动期患者中比临床缓解期患者更为明显。与非T细胞刺激的自体MLR和同种异体MLR相比，PHA - T细胞刺激的自体MLR缺陷更为明显。SLE患者和RA患者的血清对PHA诱导HLA - II类抗原、淋巴细胞对PHA的增殖反应、以PHA - T细胞和非T细胞作为刺激物的自体MLR以及同种异体MLR均未显示出任何可检测到的抑制活性。这些结果表明，我们所发现的异常反映了T细胞的内在缺陷。
