4.2 Article

Immune responses to self-antigens in asthma patients: clinical and immunopathological implications

Journal

HUMAN IMMUNOLOGY
Volume 73, Issue 5, Pages 511-516

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.humimm.2012.02.010

Keywords

Asthma; Autoimmunity; Collagen V; Epidermal growth factor receptor; Activin A type 1 receptor; alpha-Catenin

Categories

Funding

  1. NIH [UL1 R024992, HL69149, SCOR HL56419, U19-A1070489]
  2. American Lung Association Asthma Clinical Research Center
  3. Doris Duke Fellowship Grant
  4. BJC Foundation

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Asthma leads to chronic airway inflammation that shares pathological features of chronic rejection after lung transplantation. Due to the significant role of autoimmunity in chronic rejection, we hypothesized that immunity to self-antigens may also be present in asthma. The goal was to define immune responses to self-antigens in patients with asthma. Blood and clinical data were collected from 99 asthmatics and 60 controls. Serum was analyzed for antibodies (Abs) to collagen V (ColV) by enzyme-linked immunosorbent assay and correlated with disease severity. Asthmatics' sera were tested in a human protein array to determine immune responses to other self-antigens. Asthmatics had higher concentrations of Abs to ColV (predominantly immunoglobulin G isotype) compared with controls (p < 0.01). These Abs correlated with severe asthma (p < 0.01) and corticosteroid use (p = 0.032). Additionally, Abs to novel self-antigens epidermal group factor receptor (EGFr), activin A type 1 receptor, and alpha-catenin were detected in asthmatics. We conclude that Abs to self-antigens (ColV, EGFr, activin A type 1 receptor, and a-catenin) are present in the sera of asthmatics, correlating with clinical disease. Epithelial damage from airway inflammation during asthma may result in the exposure of cryptic self-antigens or their determinants, resulting in immune response to self-antigens, which may contribute to the pathogenesis of asthma. (C) 2012 American Society for Histocompatibility and lmmunogenetics. Published by Elsevier Inc. All rights reserved.

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