Beta Cells Deficient for Renalase Counteract Autoimmunity by Shaping Natural Killer Cell Activity.

ABSTRACT: Type 1 diabetes (T1D) arises from autoimmune-mediated destruction of insulin-producing pancreatic beta cells. Recent advancements in the technology of generating pancreatic beta cells from human pluripotent stem cells (SC-beta cells) have facilitated the exploration of cell replacement therapies for treating T1D. However, the persistent threat of autoimmunity poses a significant challenge to the survival of transplanted SC-beta cells. Genetic engineering is a promising approach to enhance immune resistance of beta cells as we previously showed by inactivating of the Renalase (Rnls) gene. Here we demonstrate that Rnls loss-of-function in beta cells shape autoimmunity by mediating a regulatory Natural Killer (NK) cell phenotype important for the induction of tolerogenic

SUBMITTER: Bode K 

PROVIDER: S-EPMC10942322 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature