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系统性红斑狼疮(SLE)是一种多因素疾病,其发病机制至今尚未明确。有研究表明,遗传易感性在疾病发生中起重要作用。PTPN22(蛋白酪氨酸磷酸酶非受体型22)基因作为SLE的遗传标记是一个很好的候选基因,该基因位于染色体1p13.2,编码淋巴样特异性磷酸酶,有证据表明SLE T细胞酪氨酸磷酸化异常,促进了T细胞效应器功能紊乱,最终导致SLE发病。研究PTPN22基因在SLE中的作用,对探讨SLE发病机制及基因靶向治疗具有一定意义。
SLE is a multifactorial disease whose pathogenesis is not yet known. Studies have shown that genetic predisposition plays an important role in the development of the disease. The PTPN22 (protein tyrosine phosphatase non-receptor type 22) gene is a good candidate for genetic markers of SLE, which is located on chromosome 1p13.2 and encodes a lymphoid-specific phosphatase. There is evidence that SLE T cells Abnormal tyrosine phosphorylation promotes T cell effector dysfunction and eventually leads to the onset of SLE. Studying the role of PTPN22 in SLE is of great significance in exploring the pathogenesis of SLE and gene-targeted therapy.