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Single nucleotide polymorphisms that reduce PTPN2 expression have been linked with the development of various autoimmune disorders, including type 1 diabetes. The tyrosine phosphatase PTPN2 attenuates T-cell receptor and cytokine signaling in T cells to maintain peripheral tolerance, but the extent to which PTPN2 deficiency in T cells might influence type 1 diabetes onset remains unclear. NOD mice develop spontaneous autoimmune type 1 diabetes similar to that seen in humans. In this study, T-cell PTPN2 deficiency in NOD mice markedly accelerated the onset and increased the incidence of type 1 diabetes as well as that of other disorders, including colitis and Sj\u00f6gren syndrome. Although PTPN2 deficiency in CD8+ T cells alone was able to drive the destruction of pancreatic \u03b2-cells and the onset of diabetes, T-cell\u2013specific PTPN2 deficiency was also accompanied by increased CD4+ T-helper type 1 differentiation and T-follicular-helper cell polarization and increased the abundance of B cells in pancreatic islets as seen in human type 1 diabetes. These findings causally link PTPN2 deficiency in T cells with the development of type 1 diabetes and associated autoimmune comorbidities.<\/jats:p>","DOI":"10.2337\/db18-1362","type":"journal-article","created":{"date-parts":[[2019,5,21]],"date-time":"2019-05-21T00:34:16Z","timestamp":1558398856000},"page":"1251-1266","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":46,"title":["T-Cell\u2013Specific PTPN2 Deficiency in NOD Mice Accelerates the Development of Type 1 Diabetes and Autoimmune Comorbidities"],"prefix":"10.2337","volume":"68","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5145-7180","authenticated-orcid":false,"given":"Florian","family":"Wiede","sequence":"first","affiliation":[{"name":"Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia"},{"name":"Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, Australia"},{"name":"Peter MacCallum 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