Innate immunity and intestinal microbiota in the development of Type 1 diabetes.

The incidence of Type 1 diabetes (T1D), an autoimmune disease that results from T-cell-mediated destruction of insulin-producing beta-cells has increased during the past several decades in developed countries, suggesting that changes in the environment (including the human microbial environment) may influence disease pathogenesis. This study showed that specific pathogen-free NOD mice lacking MyD88 protein (an adaptor for multiple innate immune receptors that recognise microbial stimuli) do not develop T1D. The effect is dependent on commensal microbes because germ-free MyD88-negative NOD mice develop robust diabetes, whereas colonisation of these germ-free MyD88-negative NOD mice with a defined microbial consortium (representing bacteria normally present in human gut) attenuates T1D. The authors conclude that these findings indicate that interaction of the intestinal microbes with the immune system is a critical epigenetic factor modifying T1D predisposition. Nature. 2008; Sep 21 [Epub ahead of print] .