James C. Needell

TL;DR: Data implicating the gut microbiota in disease progression is discussed with an emphasis on recent studies performed in humans and in rodent models of T1D, suggesting a causal role for the gut microbiome in islet destruction.

TL;DR: Data demonstrate that short-chain fatty acids can reshape the intestinal microbiota and prevent virus-induced islet autoimmunity and may therefore represent a useful therapeutic strategy for disease prevention.

TL;DR: The data implying that innate immune pathways are linked with mechanisms of islet autoimmunity hold great promise for the identification of novel disease pathways that may be harnessed for clinical intervention but more work needs to be done to better understand mechanisms by which innate immunity triggers β-cell destruction.

TL;DR: The studies provide evidence raising the hypothesis that visceral adipose tissue inflammation and dysfunction may be involved in early mechanisms triggering β cell autoimmunity, and proof-of-principle studies show that brief anti-inflammatory steroid therapy suppresses visceral adipOSE tissueinflammatory and protects from virus-induced disease.

TL;DR: The data suggest that ITF-2357 and Anakinra differentially influence the innate immune system and the intestinal microbiota and highlight the potential use of the gut microbiome as a surrogate means of assessing anti-inflammatory immune effects in type 1 diabetes.