Oral Infections and Autoimmune Diseases

摘要: Abstract Environmental factors such as oral infections may play an important triggering role in the pathogenesis of autoimmune diseases (AIDs) among genetically susceptible individuals. The putative pathogenic mechanism has been presented. AIDs involves naive T-cells developing into Th17 cells and leading to with help multiple transcription cytokines interferon (INF)-γ, interleukin (IL)-6, IL-21, IL-23, transforming growth factor (TGF)-β, forkhead box P3 (Foxp3). These are also expressed infections. Hence, molecular biology framework discussed. Bacterial lipopolysaccharides (LPS) recognized via toll-like receptors (TLRs) become epitopes for antibodies causing AIDs. Moreover, Porphyromonas gingivalis (P. gingivalis) is known secrete peptidylarginine deiminase, which citrullinates fibrinogen, auto-antigen rheumatoid arthritis (RA). Citrullinated enolase peptide-1 (CEP-1) B-cells α-enolase from P. showed 82–100% sequence matching. Thus, mimicry CEP-1 might be a possible connection between RA pathogenesis. Furthermore, evidence linking various diseases, including atherosclerosis, arthritis, systemic lupus erythematosus, sclerosis, antiphospholipid syndrome, Sjogren's syndrome Crohn's disease, critically reviewed individually causal context. Also discussed future directions establishing causality relationship Applying results animal, vitro or ex vivo studies humans requires careful adjustment confounding effects smoking, genetics other competing factors.