title: Autoimmune pancreatitis and complement activation system.
abstract: OBJECTIVE
  Autoimmune pancreatitis is characterized by increased serum level of IgG4, but its pathogenesis has not been fully elucidated. Because this disease is occasionally associated with decreased levels of complements, we sought to clarify which complement activation system was operating in its active state.
  
  
  METHODS
  We measured serum levels of complements, mannose-binding lectin, and circulating immune complex in patients with autoimmune pancreatitis, patients with chronic pancreatitis, and healthy controls.
  
  
  RESULTS
  We found high serum circulating immune complex values, which decreased significantly after corticosteroid therapy. In patients with autoimmune pancreatitis, elevated levels of circulating immune complex, as determined by C1q assay, were significantly associated with increased serum levels of IgG1 and decreased levels of C4, as well as with a tendency toward decreased levels of C3. There were no significant differences in the serum levels of mannose-binding lectin or in the frequency of a mutant allele of mannose-binding lectin between patients with autoimmune pancreatitis and those with chronic calcifying pancreatitis. Furthermore, corticosteroid therapy had no effect on the level of mannose-binding lectin.
  
  
  CONCLUSIONS
  Autoimmune pancreatitis exhibits a high serum circulating immune complex values in its active state, which links to a complement activation system with a classic pathway rather than the mannose-binding lectin pathway or alternative pathways.
authors.affiliation: Department of Medicine and Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Muraki
authors.forename: Hideaki
authors.initials: H
authors.lastname: Hamano
authors.forename: Yasuhide
authors.initials: Y
authors.lastname: Ochi
authors.forename: Kenichi
authors.initials: K
authors.lastname: Komatsu
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Komiyama
authors.forename: Norikazu
authors.initials: N
authors.lastname: Arakura
authors.forename: Kaname
authors.initials: K
authors.lastname: Yoshizawa
authors.forename: Masao
authors.initials: M
authors.lastname: Ota
authors.forename: Shigeyuki
authors.initials: S
authors.lastname: Kawa
authors.forename: Kendo
authors.initials: K
authors.lastname: Kiyosawa
mesh_terms: D000328:Adult; D000368:Aged; D000936:Antigen-Antibody Complex / Q000097:blood; D001327:Autoimmune Diseases / Q000097:blood* / Q000188:drug therapy / Q000276:immunology*; D002908:Chronic Disease; D003167:Complement Activation; D003165:Complement System Proteins / Q000378:metabolism; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D008297:Male; D037601:Mannose-Binding Lectin / Q000097:blood; D008875:Middle Aged; D010195:Pancreatitis / Q000097:blood* / Q000188:drug therapy / Q000276:immunology*; D011239:Prednisolone / Q000627:therapeutic use; D012016:Reference Values
chemical_list: D000936:Antigen-Antibody Complex; D005938:Glucocorticoids; D037601:Mannose-Binding Lectin; D003165:Complement System Proteins; D011239:Prednisolone