title: Autoimmune-related pancreatitis is associated with autoantibodies and a Th1/Th2-type cellular immune response.
abstract: OBJECTIVE
  Although autoimmunity may be involved in some cases of pancreatitis, the mechanism is still unknown. To clarify this, we studied serum autoantibodies, subsets of lymphocytes, and the Th1/Th2 balance of cellular immune responses in patients with autoimmune-related pancreatitis (AIP).
  
  
  METHODS
  Seventeen patients with AIP (8 men and 9 women; age, 53.2 +/- 13.0 years) were studied. Autoantibodies including antilactoferrin (ALF) or carbonic anhydrase II antibody (ACA-II) were examined using the enzyme-linked immunosorbent assay (ELISA) or the indirect fluorescein antibody method. Intracellular cytokines (interferon gamma and interleukin 4) and subtypes of peripheral blood lymphocytes were examined by flow cytometry and ELISA.
  
  
  RESULTS
  More than one autoantibody was observed in all 17 patients. Serum antinuclear antibody was detected in 13 of 17 patients, ALF antibody in 13, ACA-II antibody in 10, rheumatoid factor in 5, and anti-smooth muscle antibody in 3, but antimitochondrial antibody in none. The serum levels of ACA-II and LF antibody were not correlated. HLA-DR(+)CD8(+) and HLA-DR(+)CD4(+) cells were significantly increased in peripheral blood (P < 0.05). CD4(+) cells producing interferon gamma and the secreted levels were significantly increased compared with those in controls (P < 0.05), but interleukin 4 was not increased.
  
  
  CONCLUSIONS
  An autoimmune mechanism against CA-II or LF, and Th1-type immune response, may be involved in AIP.
authors.affiliation: Department of Gastroenterology and Endoscopic Medicine, Kyoto University Hospital, Kyoto, Japan. okak@kuhp.kyoto-u.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Okazaki
authors.forename: K
authors.initials: K
authors.lastname: Uchida
authors.forename: M
authors.initials: M
authors.lastname: Ohana
authors.forename: H
authors.initials: H
authors.lastname: Nakase
authors.forename: S
authors.initials: S
authors.lastname: Uose
authors.forename: M
authors.initials: M
authors.lastname: Inai
authors.forename: Y
authors.initials: Y
authors.lastname: Matsushima
authors.forename: K
authors.initials: K
authors.lastname: Katamura
authors.forename: K
authors.initials: K
authors.lastname: Ohmori
authors.forename: T
authors.initials: T
authors.lastname: Chiba
mesh_terms: D000328:Adult; D000368:Aged; D000917:Antibody Formation; D001323:Autoantibodies / Q000032:analysis*; D001327:Autoimmune Diseases / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D002256:Carbonic Anhydrases / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D005260:Female; D006801:Humans; D007781:Lactoferrin / Q000276:immunology; D016131:Lymphocyte Subsets / Q000473:pathology; D008297:Male; D008875:Middle Aged; D010195:Pancreatitis / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D016207:Cytokines; D007781:Lactoferrin; D002256:Carbonic Anhydrases