Prevention of Islet Inflammatory Stress with JAK1/JAK2 Inhibitors

Abstract

Introduction There is an opportunity to repurpose therapeutics from other diseases to autoimmunity and transplantation, especially when there is evidence for overlapping mechanisms. Inflammation is one of the main causes of islet damage and loss during islet isolation and transplantation, and autoimmune diabetes is associated with a pro-inflammatory environment around pancreatic islets. The JAK-STAT pathway is activated by inflammatory cytokines and is important in T cells and pancreatic beta cells, the target of T cell-mediated destruction. We tested the hypothesis that blocking the response to cytokines that activate the JAK-STAT pathway would prevent islet inflammation, using ruxolitinib,..