Abstract
The etiopathogenesis of many autoimmune disorders has not been identified. The aim of this paper is to focus on the involvement of bacterial exposure, as an environmental factor, in the pathogenesis of autoimmune pancreatitis (AIP), which is broadly categorized as autoimmune disorders involving pancreatic lesions. Avirulent and/or commensal bacteria, which may have an important role(s) as initiating/progressing factors in the pathogenesis of autoimmune disorder AIP, will be emphasized.
Highlights
AUTOIMMUNE DISEASES ASSOCIATED WITH MICROBIAL INFECTION Autoimmune diseases arise from an overactive immune response of the body against tissues normally present in the body
In Guillain–Barré syndrome (GBS), amino acid similarities exist between the gangliosides of the nerve system and the lipopolysaccharides (LPSs) of Campylobacter jejuni, suggesting that sensitization by microbes may be based on autoimmunity from molecular mimicry between bacteria and the targeted system of the host (Yuki et al, 2004; Houliston et al, 2011)
A common recent theory of the cause of autoimmune diseases is that an infectious agent triggers a cycle of events, which leads to the upregulation of the host immune response to self antigens (Aoki, 1999; Tlaskalová-Hogenova et al, 2004)
Summary
MHC-II −/− mice T-cell+ HLA-DR*0405Ab0 NOD mice Tgfbr2(fspKO) mice NOD.CD28KO mice. Salivary gland, thyroid, bile duct, kidney Pancreas Pancreas Pancreas Pancreas. Qu et al (2002) Soga et al (2009) Asada et al (2010) Nishio et al (2011) Nishio et al (2011) Suzuki et al (1993) Watanabe et al (2003)
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