Back

Calorie Restriction Up-regulates Islet PD-L1 Signaling and Decreases the Risk of Auto-immune Diabetes Onset in NOD Mice.

Cambraia, A.; Schleh, M.; Cartailler, J.-P.; Cutler, M.; dos Santos, C.; Many, G.; Kim, H.; Kim, Y.-M.; Nakayasu, E. S.; Mogilenko, D.; Arrojo e Drigo, R.

2026-02-17 cell biology
10.64898/2026.02.15.705935 bioRxiv
Show abstract

Type 1 diabetes (T1D) is an autoimmune disease where beta cells are destroyed by cytotoxic T cells. Calorie restriction (CR) enhances glucose homeostasis and promotes beta cell longevity and was used as therapeutic strategy for T1D prior to the discovery of insulin. However, a significant knowledge gap remains regarding its effects on beta cells during the pathogenesis of autoimmunity. We demonstrate that CR enhances glucose homeostasis, reduces beta cell load, and delays T1D onset in NOD mice. CR induced a largely post-mitotic beta cell state marked by selective loss of beta cell identity markers, reduced DNA damage and beta cell senescence, and increased PD-L1 within the islet microenvironment. This beta cell phenotype correlates with anti-inflammatory and exhausted immune cell states in the NOD islet. Together, these findings indicate that CR improves glucose homeostasis and remodels the islet microenvironment to promote beta cell longevity via a pro-tolerogenic immune microenvironment that reduces the risk for autoimmune diabetes.

Matching journals

The top 6 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.