WDFY4 deficiency in NOD mice ameliorates autoimmune diabetes and insulitis.

ABSTRACT: The events that initiate autoimmune diabetes in nonobese diabetic (NOD) mice remain poorly understood. CD4⁺ and CD8⁺ T cells are both required to develop disease, but their relative roles in initiating disease are unclear. To test whether CD4⁺ T cell infiltration into islets requires damage to β cells induced by autoreactive CD8⁺ T cells, we inactivated Wdfy4 in nonobese diabetic (NOD) mice (NOD.Wdfy4^-/--) using CRISPR/Cas9 targeting to eliminate cross-presentation by type 1 conventional dendritic cells (cDC1s). Similar to C57BL/6 Wdfy4^-/- mice, cDC1 in NOD.Wdfy4^-/- mice are unable to cross-present cell-associated antigens to prime CD8⁺ T cells, while cDC1 from heterozygous N

SUBMITTER: Ferris ST 

PROVIDER: S-EPMC10068798 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature