Journal article

Deficiency of the innate immune adaptor STING promotes autoreactive T cell expansion in NOD mice

Satoru Akazawa, Leanne Mackin, Gaurang Jhala, Stacey Fynch, Tara Catterall, Claudia Selck, Kate L Graham, Balasubramanian Krishnamurthy, Evan G Pappas, Chun-Ting J Kwong, Andrew PR Sutherland, Thomas WH Kay, Thomas C Brodnicki, Helen E Thomas

DIABETOLOGIA | SPRINGER | Published : 2021


AIMS/HYPOTHESIS: Stimulator of IFN genes (STING) is a central hub for cytosolic nucleic acid sensing and its activation results in upregulation of type I IFN production in innate immune cells. A type I IFN gene signature seen before the onset of type 1 diabetes has been suggested as a driver of disease initiation both in humans and in the NOD mouse model. A possible source of type I IFN is through activation of the STING pathway. Recent studies suggest that STING also has antiproliferative and proapoptotic functions in T cells that are independent of IFN. To investigate whether STING is involved in autoimmune diabetes, we examined the impact of genetic deletion of STING in NOD mice. METHODS:..

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

Awarded by JDRF Innovation Award

Awarded by JDRF

Funding Acknowledgements

This work was funded by National Health and Medical Research Council of Australia (NHMRC) Program grants (GNT1126237 and GNT1150425), a JDRF Innovation Award (1-INO-2016-218-A-N) and fellowships from the JDRF (3-PDF-2017-379-A-N) andManpei Suzuki Diabetes Foundation (SA). The St Vincent's Institute receives support from the Operational Infrastructure Support Scheme of the Government of Victoria.