Microbiome and type 1 diabetes

Abstract

The steep increase in the incidence of type 1 diabetes (T1D), in the Western world after World War II, cannot be explained solely by genetic factors but implies that this rise must be due to crucial interactions between predisposing genes and environmental changes. Three parallel phenomena in early childhood - the dynamic development of the immune system, maturation of the gut microbiome, and the appearance of the first T1D-associated autoantibodies - raise the question whether these phenomena might reflect causative relationships. Plenty of novel data on the role of the microbiome in the development of T1D has been published over recent years and this review summarizes recent findings regarding the associations between islet autoimmunity, T1D, and the intestinal microbiota.

Keywords: Dysbiosis; Microbiota; Mycobiota; Type 1 diabetes; Virome.

Fig. 1

Healthy intestinal environment (A) compared to dysbiosis (B) that leads to intestinal inflammation and emerging of autoimmunity. Abbreviations: SCFA, short-chain fatty acids; TGF-β, transforming growth factor beta; IL, interleukin; LL-37,cathelicidin-related antimicrobial peptide 37; Ref3b, regenerating islet-derived protein 3-beta; HβD2, human beta defensin-2 (HβD2); TNF_α , tumor necrosis factor alfa; IFN_γ, interferon gamma. Symbols: dendritic cell; T cell; B cell; plasma cell; Firmicutes; Bacteroides; opportunistic pathobionts; mucin metabolisers like Akkermansia muciniphila; fungi like Candida albicans; Bacteriophage; foreign antigens; self antigens.