Isotype and IgG Subclass Distribution of Autoantibody Response to Alpha-enolase Protein in Adult Patients with Severe Asthma.
10.3349/ymj.2008.49.6.923
- Author:
Hye Ah LEE
1
;
Byul KWON
;
Gyu Young HUR
;
Sung Jin CHOI
;
Dong Ho NAHM
;
Hae Sim PARK
Author Information
1. Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon, Korea. donghonahm@yahoo.co.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Asthma;
autoantibody;
IgG;
IgG subclass;
IgE
- MeSH:
Adult;
Aged;
Asthma/*enzymology/*immunology;
Autoantibodies/*blood/classification;
Autoantigens;
Case-Control Studies;
Complement Activation;
Female;
Humans;
Immunoglobulin G/blood/classification;
Immunoglobulin Isotypes/blood;
Male;
Middle Aged;
Phosphopyruvate Hydratase/*immunology;
Recombinant Proteins/immunology;
Young Adult
- From:Yonsei Medical Journal
2008;49(6):923-930
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: 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. PATIENTS AND 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. CONCLUSION: 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.
