title: Isotype and IgG subclass distribution of autoantibody response to alpha-enolase protein in adult patients with severe asthma.
abstract: OBJECTIVE
  A possible involvement of autoimmune mechanism in the pathogenesis of bronchial asthma has been proposed. Recently, alpha-enolase protein was identified as a major autoantigen recognized by circulating IgG autoantibodies in patients with severe asthma. To evaluate a possible pathogenetic significance of these autoantibodies in severe asthma, isotype (IgG, IgA, IgM, and IgE) and IgG subclass (IgG1, IgG2, IgG3, and IgG4) distributions of autoantibodies to recombinant human alpha-enolase protein were analyzed.
  
  
  METHODS
  We examined serum samples from 10 patients with severe asthma and 7 patients with mild-to-moderate asthma, and 5 healthy controls by immunoblot analysis. Severe asthma was defined as patients having at least 1 severe asthmatic exacerbation requiring an emergency department visit or admission in the last year despite continuous typical therapies.
  
  
  RESULTS
  IgG1 was the predominant IgG subclass antibody response to alpha-enolase protein in patients with severe asthma. IgG1 autoantibody to alpha-enolase protein was detected in 7 of 10 patients with severe asthma (70%), 1 of 7 patients with mild-to-moderate asthma (14.3%), and none of 5 healthy controls (0%) (chi-square test; p < 0.05). IgA, IgM, and IgE autoantibodies to alpha-enolase protein could not be detected in patients with severe asthma.
  
  
  CONCLUSIONS
  IgG1 subclass was the predominant type of autoantibody response to alpha-enolase protein in patients with severe asthma, suggests a possibility of IgG1 autoantibody-mediated complement activation in the pathogenesis of severe asthma.
authors.affiliation: Department of Allergy and Rheumatology, Ajou University School of Medicine, San 5, Wonchon-dong, Yeongtong-gu, Suwon 443-721, Korea.
authors.forename: Hye-Ah
authors.initials: HA
authors.lastname: Lee
authors.forename: Byul
authors.initials: B
authors.lastname: Kwon
authors.forename: Gyu-Young
authors.initials: GY
authors.lastname: Hur
authors.forename: Sung-Jin
authors.initials: SJ
authors.lastname: Choi
authors.forename: Dong-Ho
authors.initials: DH
authors.lastname: Nahm
authors.forename: Hae-Sim
authors.initials: HS
authors.lastname: Park
mesh_terms: D000328:Adult; D000368:Aged; D001249:Asthma / Q000201:enzymology* / Q000276:immunology*; D001323:Autoantibodies / Q000097:blood* / Q000145:classification; D001324:Autoantigens; D016022:Case-Control Studies; D003167:Complement Activation; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood / Q000145:classification; D007132:Immunoglobulin Isotypes / Q000097:blood; D008297:Male; D008875:Middle Aged; D010751:Phosphopyruvate Hydratase / Q000276:immunology*; D011994:Recombinant Proteins / Q000276:immunology; D055815:Young Adult
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D007074:Immunoglobulin G; D007132:Immunoglobulin Isotypes; D011994:Recombinant Proteins; D010751:Phosphopyruvate Hydratase