Figure 3.

Alterations in the microbiota may promote autoimmunity through different mechanisms. Alterations of intestinal permeability caused by diet, bacterial metabolites, dysbiosis or pathobionts might increase exposure of gut microbial antigens to the gut associated lymphoid tissue. These adverse events have been associated with various autoimmune disorders through different mechanisms. Induction of Th17/Th1 cell responses, impaired or low levels of IL10-secreting Treg cell types, epitope spreading, dual TCR recognition or antigenic mimicry are some of the mechanisms. T1D, type 1 diabetes; AIG, autoimmune gastritis; IBD, inflammatory bowel disease; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus; PBC, primary biliary cholangitis; MS, multiple sclerosis; SCFA, short chain fatty acids; MS, multiple sclerosis; β2-GPI, β2-glycoprotein I; APS, anti-phospholipid syndrome; PDC-E2, pyruvate dehydrogenase complex; GDP-L-FS, guanosine diphosphate-L-fucose synthase; RPL23A, arthritis-related autoantigen 60S ribosomal protein L23a; IGRP, islet-specific glucose-6-phosphatase catalytic subunit-related protein.