Ueda Y, Murakawa Y, Takeno M, Miki T, Sakane T
Department of Internal Medicine, Shimane Medical University, Izumo-city.
Ryumachi. 1990 Oct;30(5):350-5.
We have previously shown that when patients with active rheumatoid arthritis (RA) were examined for the ability of their lymphocytes to respond in the autologous mixed lymphocyte reaction (AMLR), profoundly reduced AMLR responses were found in the RA patients. The defects were mainly due to the impaired response of CD8+ and CD4+ Law8- subsets; however, both CD4+Leu8+ and CD4+ + Leu8- cells functioned normally as responding cells. The present study demonstrated that the abnormalities of RA CD8+ T cells in the AMLR were corrected when the AMLR cultures were set up in the presence of methyl-B12. In addition, a main target of the methyl-B12 effect observed was both CD8+Leu8+ and CD8+Leu8- cells. Thus, methyl-B12 may become a potential agent that would be able to control the pathophysiology of RA.
我们之前已经表明，当对活动性类风湿关节炎（RA）患者的淋巴细胞在自体混合淋巴细胞反应（AMLR）中的反应能力进行检测时，发现RA患者的AMLR反应显著降低。这些缺陷主要是由于CD8 +和CD4 + Leu8 -亚群的反应受损；然而，CD4 + Leu8 +和CD4 + Leu8 -细胞作为反应细胞功能正常。本研究表明，当在存在甲基维生素B12的情况下建立AMLR培养物时，RA患者CD8 + T细胞在AMLR中的异常得到纠正。此外，观察到的甲基维生素B12作用的主要靶点是CD8 + Leu8 +和CD8 + Leu8 -细胞。因此，甲基维生素B12可能成为一种能够控制RA病理生理学的潜在药物。
