Goto M, Zvaifler N J
Arthritis Rheum. 1985 Jul;28(7):731-41. doi: 10.1002/art.1780280703.
Natural killer-like cells are generated along with interleukin-2 (IL-2) in the autologous mixed leukocyte reaction (AMLR). Patients with active rheumatoid arthritis (RA), but not those whose disease is in remission, are poor producers of AMLR killer cells. This defect cannot be explained by age, medications, or serum factors. The impaired generation of natural killer-like cells was not influenced by gamma-interferon but could be partially restored by addition of indomethacin to the AMLR culture, or by culturing RA T cells with exogenous IL-2. However, the response of RA T cells to IL-2 was significantly less than that of controls. These results suggest that the defect in the generation of AMLR killer cells in patients with active RA may be due in part to defective production of IL-2 and a lesser sensitivity of RA T cells to IL-2.
自然杀伤样细胞在自体混合淋巴细胞反应（AMLR）中与白细胞介素-2（IL-2）一起产生。活动性类风湿关节炎（RA）患者而非病情缓解患者是AMLR杀伤细胞的低产者。这种缺陷不能用年龄、药物或血清因子来解释。自然杀伤样细胞生成受损不受γ干扰素影响，但在AMLR培养中加入吲哚美辛，或用外源性IL-2培养RA T细胞可部分恢复。然而，RA T细胞对IL-2的反应明显低于对照组。这些结果表明，活动性RA患者AMLR杀伤细胞生成缺陷可能部分归因于IL-2产生缺陷以及RA T细胞对IL-2的敏感性较低。
