Mustelin Tomas
Program on Inflammatory Disease Research Infectious and Inflammatory Disease Center, The Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Semin Immunol. 2006 Aug;18(4):254-60. doi: 10.1016/j.smim.2006.03.013. Epub 2006 May 5.
The discovery that a single amino acid substitution in the PTPN22 protein tyrosine phosphatase can predispose to so many autoimmune diseases (see chapters 2 and 3), even when present in a single copy, raises many questions regarding the broader significance of this observation. Is there something unique about PTPN22 or are genetic variants of other protein tyrosine phosphatases likely also associated with autoimmune disease? If so, will polymorphisms in other phosphatases be found in the same spectrum of diseases? Are protein tyrosine phosphatases like PTPN22 good drug targets for the treatment of human autoimmunity? In this review, I offer some basis for thinking about these questions.
发现蛋白酪氨酸磷酸酶PTPN22中单个氨基酸的替换即便以单拷贝形式存在也会使人易患多种自身免疫性疾病（见第2章和第3章），这引发了许多关于该观察结果更广泛意义的问题。PTPN22有什么独特之处，还是其他蛋白酪氨酸磷酸酶的基因变体也可能与自身免疫性疾病有关？如果是这样，在相同疾病谱中会发现其他磷酸酶的多态性吗？像PTPN22这样的蛋白酪氨酸磷酸酶是治疗人类自身免疫性疾病的良好药物靶点吗？在这篇综述中，我为思考这些问题提供了一些依据。
