Journal article

T-Cell-Specific PTPN2 Deficiency in NOD Mice Accelerates the Development of Type 1 Diabetes and Autoimmune Comorbidities

Florian Wiede, Thomas C Brodnicki, Pei Kee Goh, Yew A Leong, Gareth W Jones, Di Yu, Alan G Baxter, Simon A Jones, Thomas WH Kay, Tony Tiganis

DIABETES | AMER DIABETES ASSOC | Published : 2019

Abstract

Genome-wide association studies have identified PTPN2 as an important non-MHC gene for autoimmunity. 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..

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Grants

Awarded by National Health and Medical Research Council (NHMRC) of Australia


Awarded by Versus Arthritis


Awarded by NHMRC


Funding Acknowledgements

This work was supported by the National Health and Medical Research Council (NHMRC) of Australia (1047055 to T.T.), Versus Arthritis (19796, 20770 to S.A.J. and G.W.J), and the Victorian Operational Infrastructure Support Program (to T.C.B. and T.W.H.K). T.T is an NHMRC Principal Research Fellow (1103037).