Cross S M, Hazelton R A
Ann Rheum Dis. 1985 Apr;44(4):224-31. doi: 10.1136/ard.44.4.224.
The response of peripheral blood lymphocytes (PBL) to autologous synovial fluid lymphocytes (SFL) from patients with rheumatoid arthritis and Reiter's syndrome was investigated in an autologous mixed lymphocyte reaction (AMLR). SFL were found to be poor responders but strong stimulators of autologous and allogeneic PBL compared with autologous PBL. The plastic-adherent (macrophage) cells from the SFL were found to be highly stimulatory to autologous PBL, particularly when the adherent cells were removed from the responding PBL. The stimulation of these PBL non-adherent cells by SFL adherent cells follows two main trends: either no stimulation, or higher stimulation than using unseparated SFL and PBL. Patients in the high stimulator group were taking non-steroidal anti-inflammatory drugs while those in the low responder group were taking, in addition, second-line drugs such as D-penicillamine or gold. Autologous serum was found to inhibit the AMLR and this is probably due to drug metabolites in patients' sera. Initial results show that the AMLR in individual patients is highly correlated, over time, with the erythrocyte sedimentation rate (ESR).
在自身混合淋巴细胞反应（AMLR）中，研究了类风湿性关节炎和赖特综合征患者外周血淋巴细胞（PBL）对自身滑膜液淋巴细胞（SFL）的反应。与自身PBL相比，发现SFL是自身和同种异体PBL的弱反应者但强刺激物。发现来自SFL的塑料贴壁（巨噬细胞）细胞对自身PBL具有高度刺激性，特别是当贴壁细胞从反应性PBL中去除时。SFL贴壁细胞对这些PBL非贴壁细胞的刺激遵循两个主要趋势：要么无刺激，要么比使用未分离的SFL和PBL有更高的刺激。高刺激组的患者正在服用非甾体抗炎药，而低反应组的患者除了服用二线药物如D-青霉胺或金制剂外还服用其他药物。发现自身血清可抑制AMLR，这可能是由于患者血清中的药物代谢产物所致。初步结果表明，随着时间的推移，个体患者的AMLR与红细胞沉降率（ESR）高度相关。
