title: Possible involvement of Toll-like receptor 7 in the development of type 1 autoimmune pancreatitis.
abstract: BACKGROUND
  High serum immunoglobulin G4 (IgG4) levels and IgG4-positive plasma cell infiltration are characteristic of type 1 autoimmune pancreatitis (AIP). It is unclear whether innate immunity is a cause of type 1 AIP; the possible involvement of microbial infection has been suggested in its pathogenesis. To clarify the pathogenesis of type 1 AIP, we investigated Toll-like receptors (TLRs) in type 1 AIP patients.
  
  
  METHODS
  We studied nine cases of type 1 AIP with ten cases of alcoholic chronic pancreatitis (ACP) and three of the samples from non-tumorous lesion of neuroendocrine tumor (NET) as control subjects. We counted the number of TLR1-11-positive cells immunohistochemically stained with anti-TLR1-11 antibodies. To identify TLR-positive cells in pancreata from type 1 AIP patients, we used a double-immunofluorescence method and counted the numbers of identifiable CD68-, CD163-, CD123-, and CD20-positive cells.
  
  
  RESULTS
  In type 1 AIP, TLR7 (8.815 ± 1.755), TLR8 (3.852 ± 1.489), and TLR10 (3.852 ± 0.921) were highly expressed. Only the ratio of TLR7 per monocyte was significantly higher in type 1 AIP (0.053 ± 0.012) than in ACP (0.007 ± 0.004; p < 0.01) and non-tumorous lesion of NET (0.000 ± 0.000; p < 0.01). In type 1 AIP, the CD163 to TLR7 ratio (0.789 ± 0.031) was significantly higher both than that of CD123 to TLR7 ratio (0.034 ± 0.006; p < 0.001) and CD20 to TLR7 ratio (0.029 ± 0.010; p < 0.001).
  
  
  CONCLUSIONS
  TLR7 might be key pattern-recognition receptors involved in the development of type 1 AIP.
authors.affiliation: Division of Gastroenterology and Hepatology, The Third Department of Internal Medicine, Kansai Medical University, 2-5-1 Shinmachi, Hirakata, Osaka, 573-1010, Japan.
authors.forename: Yuri
authors.initials: Y
authors.lastname: Fukui
authors.forename: Kazushige
authors.initials: K
authors.lastname: Uchida
authors.forename: Yutaku
authors.initials: Y
authors.lastname: Sakaguchi
authors.forename: Toshiro
authors.initials: T
authors.lastname: Fukui
authors.forename: Akiyoshi
authors.initials: A
authors.lastname: Nishio
authors.forename: Nobuaki
authors.initials: N
authors.lastname: Shikata
authors.forename: Noriko
authors.initials: N
authors.lastname: Sakaida
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Uemura
authors.forename: Sohei
authors.initials: S
authors.lastname: Satoi
authors.forename: Kazuichi
authors.initials: K
authors.lastname: Okazaki
mesh_terms: D000328:Adult; D000368:Aged; D001327:Autoimmune Diseases / Q000276:immunology* / Q000473:pathology; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007113:Immunity, Innate; D008297:Male; D008875:Middle Aged; D010179:Pancreas / Q000276:immunology; D019512:Pancreatitis, Alcoholic / Q000276:immunology; D050500:Pancreatitis, Chronic / Q000276:immunology* / Q000473:pathology; D051199:Toll-Like Receptor 7 / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology
chemical_list: C495348:TLR7 protein, human; D051199:Toll-Like Receptor 7; D051193:Toll-Like Receptors