Autoimmune pancreatitis in Japan: overview and perspective

Abstract

Since the rediscovery and definition of autoimmune pancreatitis (AIP) by Yoshida et al. in 1995, the disease has been attracting attention because of its unique clinical features and practical issues. This disease shows very impressive imaging findings, serological changes, and characteristic histopathology. It occurs most commonly in elderly males with painless jaundice or mild abdominal pain; resemblance in imaging findings between AIP and pancreatobiliary cancers poses an important practical issue of differentiation. With increasing recognition of AIP and accumulation of cases, another important feature of this disease has been revealed, i.e

A mouse model of autoimmune pancreatitis with salivary gland involvement triggered by innate immunity via persistent exposure to avirulent bacteria

“…[4][5][6] Recently, growing evidence suggests that two clinical and histological patterns of AIP exist (i) lymphoplasmacytic sclerosing pancreatitis (LPSP) or type 1 AIP, which fits the classic description of disease reported from Japan; and (ii) idiopathic duct-centric pancreatitis (IDCP) or type 2 AIP, which is characterized by granulocyte epithelial lesions (GEL) in the pancreas (see Park et al 5 and references therein). IDCP or AIP with GEL is characterized by the massive infiltration of granulocytes in the pancreatic parenchyma and ductal epithelium.…”

“…Together, AIP with GEL has different clinical characteristics from AIP with LPSP. 6 The pathogenesis of AIP remains unknown. 4,5 The concept of a syndrome complex or autoimmune exocrinopathy suggests that the pancreas and other organs may possess common target antigens.…”

“…4,5 The concept of a syndrome complex or autoimmune exocrinopathy suggests that the pancreas and other organs may possess common target antigens. 6 A close association with the human leukocyte antigen (HLA) haplotypes DRB1*0405 and DQB1*0401 has been reported in AIP patients. 7,8 Thus, the antigen presentation of some common peptide to T cells through HLA DRB1*0405 or HLA DQB1*0401 might trigger AIP.…”

“…9 Anti-carbonic anhydrase II (anti-CA-II) and -lactoferrin (anti-LF) are the most frequently detected autoantibodies in human AIP. [4][5][6] Although anti-CA-II and anti-LF are frequently positive in LPSP, they are rarely positive in IDCP. 5 These autoantibodies might also be involved in the pathogenesis of AIP.…”

“…[4][5][6] To determine whether AIP mouse model triggered by bacteria I Haruta et al autoantibodies are generated in repeated E. coli-inoculated C57BL/6 mice in vivo, anti-CA-II and anti-LF antibodies were measured. The anti-CA-II antibody levels in sera from C57BL/6 mice inoculated with E. coli were significantly higher than those in mice inoculated with PBS.…”