Fig. 3

The critical mechanism of oral microorganisms in autoimmune diseases. The major pathways of oral microorganisms-autoimmune diseases axis are shown among the microbiota translocation, molecular mimicry, autoantigen overproduction and amplification of autoimmunity by cytokine. Top left: communication between oral microbiota and the host involves the hematogenous and enteral routes. Under the adverse conditions such Ulcers and periodontal destruction, oral microbiome, such as P.g, S.mutans, and other periodontal pathogens arrive at the distant organs, subsequently increasing the release of cytokines and affecting intestinal barrier integrity. Change in the oral microbiota composition can also increase the response of molecular mimicry, autoantigen overproduction and amplification of autoimmunity by cytokine. Top right: the antigen epitopes of P. denticola, B. cereus, P.gingivalis, F.nucleatum, and Streptococcus increase. Bottom left: The production of residual and citrullinated epitope increase due to the hydrolysis of enzymes form microorganisms. The epitopes might be preferentially captured by APC which presented antigen epitopes to T cells, leading to the production of inflammatory factors. Subsequently, B cell response is activated to produce antibodies. Bottom right: Pathogenic microorganisms including P. gingivalis, F. nucleatum and C. concisus promote the release of TH1/TH17, TNFα, IFNα, Ilβ, IL-6, IL-17. p.g, P.gingivalis; k.s, Klebsiella strains; c.c, C. concisus; APC, Antigen presenting cell; TLR, Toll-like receptor; RA, Rheumatoid arthritis; IBD, Inflammatory bowel disease; Ro60, Anti-dsDNA, Anti-double stranded DNA antibody; Ro60, Ro ribonucleoprotein 60 KDa; PDC-E2, Pyruvate dehydrogenase complex E2