摘要
目的观察白细胞介素(IL)-2作用于类风湿关节炎(RA)与骨关节炎(OA)外周血T淋巴细胞前后,T淋巴细胞中STAT3及STAT5的酪氨酸磷酸化活化状态,并进行比较。方法从RA与OA患者的外周血中分离培养单个核细胞,继而纯化得到T淋巴细胞,静息后,用重组人IL-2刺激,在各时相裂解细胞,收获提取蛋白,进行Westernblot分析。结果在静息后,RA与OA的外周血T淋巴细胞中STAT3与STAT5均处于极低水平磷酸化的状态;在IL-2作用后,T淋巴细胞中STAT3和STAT5发生时相性的酪氨酸磷酸化,而RA的T淋巴细胞磷酸化程度较OA显著增高。结论IL-2对RA患者T淋巴细胞的STAT3和STAT5过度激活,引起T淋巴细胞中IL-2信号传导的异常放大效应,可能在RA的发病过程中发挥重要作用。
Objective To compare tyrosine phosphorylation of STAT3 and STAT5 induced by IL-2 in T-lymphocytes from peripheral blood of patients with rheumatoid arthritis （RA） and osteoarthritis （OA）. Methods Peripheral blood mononuclear cells （PBMCs） were isolated from RA and OA patients, then T-lymphocytes purified from PBMCs were stimulated by rhlL-2. Total proteins of T cells were extracted after different time intervals. Results After rest, the tyrosine phosphorylation of STAT3 and STATS in T-lymphocytes from both RA and OA patients were at extremely low level. After stimulated with IL-2, tyrosine phosphorylation of both STAT3 and STAT5 in T cells from RA were time dependent and the phosphorylation was prominent than that from OA. Conclusion Even in RA, STAT3 and STAT5 pathway in T-lymphocytes from peripheral blood can not he automatically activated. The excessive tyrosine phosphorylation of STAT3 and STATS in RAT cells probably amplify the downstream signal transduction of IL-2, thus lead to an enhancement of transcription of certain genes, which seem to play some important roles in the pathogenesis of RA.
出处
《中华风湿病学杂志》
CAS
CSCD
2005年第10期590-593,共4页
Chinese Journal of Rheumatology
基金
北京大学211重点学科基金资助项目(904)
