Leeds Institute of Cancer and Pathology, St James's University Hospital, University of Leeds, Leeds, UK.
Ashworth Laboratories, Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh, UK.
Immunology. 2018 Jul;154(3):377-382. doi: 10.1111/imm.12919. Epub 2018 Apr 16.
A number of polymorphisms in immune-regulatory genes have been identified as risk factors for the development of autoimmune disease. PTPN22 (that encodes a tyrosine phosphatase) has been associated with the development of several autoimmune diseases, including type 1 diabetes, rheumatoid arthritis and systemic lupus erythematosus. PTPN22 regulates the activity and effector functions of multiple important immune cell types, including lymphocytes, granulocytes and myeloid cells. In this review, we describe the role of PTPN22 in regulating T-cell activation and effector responses. We discuss progress in our understanding of the impact of PTPN22 in autoimmune disease in humans and mouse models, as well as recent evidence suggesting that genetic manipulation of PTPN22 expression might enhance the efficacy of anti-tumour T-cell responses.
许多免疫调节基因的多态性已被确定为自身免疫性疾病发展的风险因素。PTPN22（编码一种酪氨酸磷酸酶）与多种自身免疫性疾病的发展有关，包括 1 型糖尿病、类风湿关节炎和系统性红斑狼疮。PTPN22 调节多种重要免疫细胞类型的活性和效应功能，包括淋巴细胞、粒细胞和髓样细胞。在这篇综述中，我们描述了 PTPN22 在调节 T 细胞激活和效应应答中的作用。我们讨论了我们对 PTPN22 在人类和小鼠模型中自身免疫性疾病的影响的理解的进展，以及最近的证据表明，遗传操纵 PTPN22 表达可能增强抗肿瘤 T 细胞应答的疗效。
