Tosato G, Steinberg A D, Yarchoan R, Heilman C A, Pike S E, De Seau V, Blaese R M
J Clin Invest. 1984 Jun;73(6):1789-95. doi: 10.1172/JCI111388.
Patients with rheumatoid arthritis (RA) are known to have in vitro regulatory T cell abnormalities relating to Epstein-Barr virus (EBV). In this report, we asked whether patients with RA have more circulating EBV-infected B cells than normals. To address this question, we determined the frequency of spontaneously transforming B cells in the peripheral blood of 18 normals, 15 patients with RA, and 8 patients with systemic lupus erythematosus (SLE). The mean frequency of spontaneously transforming B cells in RA patients was 10.1/10(6) B cells, which was significantly greater than that of the normal controls, 2.8/10(6) B cells (P less than 0.005). The group of patients with SLE did not differ from the normals (P greater than 0.4). In further studies undertaken to investigate as to whether RA B cells are more easily transformed by EBV than normal B cells, we determined that the frequencies of transforming B cells in the presence of exogenous EBV were similar in RA patients and normals. Lymphocytes obtained from patients with RA demonstrate a profound T cell defect in their EBV-specific suppression, as measured in vitro; there was no direct correlation, however, between this in vitro T cell abnormality and the number of circulating EBV-infected B cells. Thus, patients with RA, as a group, have abnormally elevated numbers of circulating EBV-infected B cells, and this abnormality most likely derives from a complex dysregulation of the defense mechanisms for infection with EBV.
已知类风湿关节炎(RA)患者存在与爱泼斯坦-巴尔病毒(EBV)相关的体外调节性T细胞异常。在本报告中,我们探讨了RA患者循环中受EBV感染的B细胞数量是否多于正常人。为解决这个问题,我们测定了18名正常人、15名RA患者和8名系统性红斑狼疮(SLE)患者外周血中自发转化B细胞的频率。RA患者自发转化B细胞的平均频率为10.1/10⁶ B细胞,显著高于正常对照组的2.8/10⁶ B细胞(P<0.005)。SLE患者组与正常人无差异(P>0.4)。在进一步研究RA B细胞是否比正常B细胞更容易被EBV转化时,我们发现RA患者和正常人在外源性EBV存在时转化B细胞的频率相似。从RA患者获得的淋巴细胞在体外检测中显示出EBV特异性抑制方面存在严重的T细胞缺陷;然而,这种体外T细胞异常与循环中受EBV感染的B细胞数量之间没有直接相关性。因此总体而言,RA患者循环中受EBV感染的B细胞数量异常升高,这种异常很可能源于EBV感染防御机制的复杂失调。