Isomäki P, Söderström K O, Punnonen J, Roivainen A, Luukkainen R, Merilahti-Palo R, Nikkari S, Lassila O, Toivanen P
Turku Immunology Centre, Turku University, Finland.
Br J Rheumatol. 1996 Jul;35(7):611-9. doi: 10.1093/rheumatology/35.7.611.
Since defective apoptosis has been suggested to play a role in the development of autoimmune diseases, we have investigated the expression of the proto-oncogene bcl-2 in patients with rheumatoid arthritis (RA). The expression of bcl-2 was studied in peripheral blood (PB) and synovial fluid (SF) lymphocytes and synovial tissues (ST) from patients with RA using immunohistochemistry, flow cytometry and nucleic acid hybridization. Patients with reactive arthritis (ReA) or osteoarthritis (OA) and healthy individuals were used as controls. The expression of bcl-2 protein in PB lymphocytes and the expression of bcl-2 mRNA in PB mononuclear cells (PBMC) was similar in healthy controls and patients with RA. However, bcl-2 protein expression was significantly reduced in SF lymphocytes when compared to PB lymphocytes. Similar results were observed with lymphocytes from patients with ReA, and irrespective of whether total lymphocytes, T cells or different T-cell subsets were studied. In the synovial sections, the expression of bcl-2 was restricted to lymphocytes, and bcl-2+ cells were observed in the majority of samples from patients with RA, OA and ReA. These data indicate that the expression of bcl-2 is not increased in the lymphocytes or ST derived from patients with RA. Instead, decreased expression of bcl-2 protein in SF lymphocytes compared to PB lymphocytes was demonstrated. We suggest that bcl-2 does not play a significant role in the pathogenesis of RA.
由于有研究表明凋亡缺陷在自身免疫性疾病的发展中起作用，我们研究了类风湿关节炎（RA）患者中原癌基因bcl-2的表达。使用免疫组织化学、流式细胞术和核酸杂交技术，对RA患者的外周血（PB）、滑膜液（SF）淋巴细胞及滑膜组织（ST）中bcl-2的表达进行了研究。以反应性关节炎（ReA）或骨关节炎（OA）患者及健康个体作为对照。健康对照和RA患者外周血淋巴细胞中bcl-2蛋白的表达以及外周血单个核细胞（PBMC）中bcl-2 mRNA的表达相似。然而，与外周血淋巴细胞相比，滑膜液淋巴细胞中bcl-2蛋白表达显著降低。ReA患者的淋巴细胞也观察到类似结果，且无论研究的是总淋巴细胞、T细胞还是不同的T细胞亚群。在滑膜切片中，bcl-2的表达局限于淋巴细胞，在大多数RA、OA和ReA患者的样本中均观察到bcl-2阳性细胞。这些数据表明，RA患者的淋巴细胞或滑膜组织中bcl-2的表达并未增加。相反，与外周血淋巴细胞相比，滑膜液淋巴细胞中bcl-2蛋白表达降低。我们认为bcl-2在RA的发病机制中不起重要作用。
