| First Author | Rui J | Year | 2021 |
| Journal | Nat Commun | Volume | 12 |
| Issue | 1 | Pages | 5074 |
| PubMed ID | 34417463 | Mgi Jnum | J:330916 |
| Mgi Id | MGI:6754023 | Doi | 10.1038/s41467-021-25367-z |
| Citation | Rui J, et al. (2021) Tet2 Controls the Responses of beta cells to Inflammation in Autoimmune Diabetes. Nat Commun 12(1):5074 |
| abstractText | beta cells may participate and contribute to their own demise during Type 1 diabetes (T1D). Here we report a role of their expression of Tet2 in regulating immune killing. Tet2 is induced in murine and human beta cells with inflammation but its expression is reduced in surviving beta cells. Tet2-KO mice that receive WT bone marrow transplants develop insulitis but not diabetes and islet infiltrates do not eliminate beta cells even though immune cells from the mice can transfer diabetes to NOD/scid recipients. Tet2-KO recipients are protected from transfer of disease by diabetogenic immune cells.Tet2-KO beta cells show reduced expression of IFNgamma-induced inflammatory genes that are needed to activate diabetogenic T cells. Here we show that Tet2 regulates pathologic interactions between beta cells and immune cells and controls damaging inflammatory pathways. Our data suggests that eliminating TET2 in beta cells may reduce activating pathologic immune cells and killing of beta cells. |
