title: The clinical significance of IgA antimitochondrial antibodies in sera and saliva in primary biliary cirrhosis.
abstract: It still remains unclear how antimitochondrial autoantibodies (AMA) are involved with immunopathogenesis of primary biliary cirrhosis (PBC). We have suggested the potential role of IgA-AMA in damage to epithelial cells in PBC. In the current study, we investigated whether IgA-AMA were detectable in sera and saliva of PBC patients, to examine the association between detectable IgA-type autoantibodies in sera or saliva and progression of liver diseases. Fifty-three patients with PBC were enrolled, and IgA-AMA in sera and saliva were sought by immunoblotting using pork heart mitochondria as antigens. The progression of PBC was determined as Scheuer's classification consisting of four histological stages. We found IgA-AMA, IgA-anti-PDC-E2, and IgA-anti-E3BP in 43/53 (81%), 37/53 (70%), and 35/53 (66%) sera of patients with PBC, but none of controls. The progression of PBC was statistically associated with presence of IgA-anti-PDC-E2 (P = 0.0124), but neither with IgA-AMA (P = 0.1296) nor anti-IgA-E3BP (P = 0.5973). In saliva, detectable IgA-AMA, IgA-anti-PDC-E2, and IgA-anti-E3BP were noted in 12/26 (46%), 6/26 (23%), and 11/26 (42%), respectively. Detection of IgA-anti-PDC-E2 was strongly associated with progression of PBC (P = 0.0002), whereas detection of IgA-AMA and IgA-anti-E3BP were not associated (P = 0.2145 and P = 0.5118). The current findings suggest that the presence of IgA-anti-PDC-E2 in sera or saliva might be associated with progression of PBC, although a prospective study with PBC patients with detectable IgA-anti-PDC-E2 at early stages will be required to conclude the contribution of IgA-anti-PDC-E2 to the progression of PBC.
authors.affiliation: Department of Medicine, Teikyo University School of Medicine, 2-11-1, Kaga, Itabashi-ku, Tokyo 173-8605, Japan. a-tanaka@med.teikyo-u.ac.jp
authors.forename: Atsushi
authors.initials: A
authors.lastname: Tanaka
authors.forename: Saeko
authors.initials: S
authors.lastname: Nezu
authors.forename: Satoko
authors.initials: S
authors.lastname: Uegaki
authors.forename: Masaki
authors.initials: M
authors.lastname: Mikami
authors.forename: Shuhei
authors.initials: S
authors.lastname: Okuyama
authors.forename: Naohiro
authors.initials: N
authors.lastname: Kawamura
authors.forename: Mitsuhiko
authors.initials: M
authors.lastname: Aiso
authors.forename: M Eric
authors.initials: ME
authors.lastname: Gershwin
authors.forename: Shin-Ichi
authors.initials: S
authors.lastname: Takahashi
authors.forename: Carlo
authors.initials: C
authors.lastname: Selmi
authors.forename: Hajime
authors.initials: H
authors.lastname: Takikawa
mesh_terms: D018450:Disease Progression; D005260:Female; D006801:Humans; D007070:Immunoglobulin A / Q000276:immunology* / Q000378:metabolism*; D007071:Immunoglobulin A, Secretory / Q000276:immunology*; D008105:Liver Cirrhosis, Biliary / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D008928:Mitochondria / Q000276:immunology*; D012463:Saliva / Q000276:immunology*; D012859:Sjogren's Syndrome / Q000175:diagnosis / Q000276:immunology