Wang M, Zhang W, Zhang Yuanchao
Department of Rheumatology and Immunology, Provincial Hospital affiliated to Shandong University, Jinan, China.
J Int Med Res. 2009 Sep-Oct;37(5):1293-300. doi: 10.1177/147323000903700504.
This study analysed the expression and activation of proline-rich tyrosine kinase 2 (PYK2) in peripheral blood mononuclear cells (PBMCs) from 36 systemic lupus erythematosus (SLE) patients and explored whether activation of PYK2 correlates with disease activity or organ damage in SLE. Samples from 19 patients with rheumatoid arthritis (RA) and 15 healthy individuals were included as controls. There was a significant increase in both total PYK2 protein and its activated/phosphorylated form in PBMCs from patients with SLE, particularly in those with the complication of World Health Organization class IV lupus nephritis. There was a clear correlation between the activation of PYK2 and the level of serum complement, but no relationship was found between the activation of PYK2 and SLE Disease Activity Index (SLEDAI). As previous studies have shown that PYK2 provides important signals during the activation of lymphocytes, PYK2 could be a major contributor to the complex autoimmune pathogenesis of SLE.
本研究分析了36例系统性红斑狼疮(SLE)患者外周血单个核细胞(PBMC)中富含脯氨酸的酪氨酸激酶2(PYK2)的表达及激活情况,并探讨PYK2的激活是否与SLE的疾病活动度或器官损伤相关。纳入19例类风湿关节炎(RA)患者和15名健康个体的样本作为对照。SLE患者PBMC中的总PYK2蛋白及其激活/磷酸化形式均显著增加,尤其是那些伴有世界卫生组织IV级狼疮性肾炎并发症的患者。PYK2的激活与血清补体水平之间存在明显相关性,但未发现PYK2的激活与SLE疾病活动指数(SLEDAI)之间存在关联。正如先前研究表明PYK2在淋巴细胞激活过程中提供重要信号一样,PYK2可能是SLE复杂自身免疫发病机制的主要促成因素。