TY - JOUR
T1 - Immune responses to self-antigens in asthma patients
T2 - Clinical and immunopathological implications
AU - Liu, Michael
AU - Subramanian, Vijay
AU - Christie, Chandrika
AU - Castro, Mario
AU - Mohanakumar, Thallachallour
N1 - Funding Information:
This publication was made possible by an award from the NIH UL1 R024992, HL69149, SCOR HL56419, U19-AI070489, and an American Lung Association Asthma Clinical Research Center grant (MC). The contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH. ML was supported by the Doris Duke Fellowship Grant. TM is supported by the BJC Foundation. The authors thank Ms. Billie Glasscock for assistance in preparing the manuscript.
PY - 2012/5
Y1 - 2012/5
N2 - 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 α-catenin were detected in asthmatics. We conclude that Abs to self-antigens (ColV, EGFr, activin A type 1 receptor, and α-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.
AB - 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 α-catenin were detected in asthmatics. We conclude that Abs to self-antigens (ColV, EGFr, activin A type 1 receptor, and α-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.
KW - Activin A type 1 receptor
KW - Asthma
KW - Autoimmunity
KW - Collagen V
KW - Epidermal growth factor receptor
KW - α-Catenin
UR - http://www.scopus.com/inward/record.url?scp=84860229954&partnerID=8YFLogxK
U2 - 10.1016/j.humimm.2012.02.010
DO - 10.1016/j.humimm.2012.02.010
M3 - Article
C2 - 22386692
AN - SCOPUS:84860229954
SN - 0198-8859
VL - 73
SP - 511
EP - 516
JO - Human Immunology
JF - Human Immunology
IS - 5
ER -