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Unraveling the functional implications of GWAS: how T cell protein tyrosine phosphatase drives autoimmune disease
Julie Zikherman, Arthur Weiss
Julie Zikherman, Arthur Weiss
Published November 14, 2011
Citation Information: J Clin Invest. 2011;121(12):4618-4621. https://doi.org/10.1172/JCI60001.
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Commentary

Unraveling the functional implications of GWAS: how T cell protein tyrosine phosphatase drives autoimmune disease

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Abstract

Genome-wide association studies (GWAS) have identified a large number of SNPs that are linked to human autoimmune diseases. However, the functional consequences of most of these genetic variations remain undefined. T cell protein tyrosine phosphatase (TCPTP, which is encoded by PTPN2) is a JAK/STAT and growth factor receptor phosphatase that has been linked to the pathogenesis of type 1 diabetes, rheumatoid arthritis, and Crohn’s disease by GWAS. In this issue of the JCI, Wiede and colleagues have generated a T cell–specific deletion of TCPTP and identified a novel role for this phosphatase as a negative regulator of TCR signaling. These data provide new insight as to how noncoding PTPN2 SNPs identified in GWAS could drive human autoimmune diseases.

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Julie Zikherman, Arthur Weiss

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