Adaptive Immune Responses of Patients with Asthma to the Attachment (G) Glycoprotein of Respiratory Syncytial Virus
Author(s) -
Gerald E. Hancock,
Catherine Scheuer,
Renata Sierzega,
Karin Pryharski,
John T. McBride,
Luc F. Miller Watelet,
Paul W. Tebbey,
Jason D. Smith
Publication year - 2001
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/324583
Subject(s) - immunology , asthma , pathogenesis , immune system , peripheral blood mononuclear cell , bronchiolitis , medicine , glycoprotein , eosinophilia , respiratory system , virus , biology , biochemistry , microbiology and biotechnology , in vitro
A history of acute bronchiolitis in infancy caused by respiratory syncytial virus is a risk factor for recurrent wheezing in early childhood. Because the attachment (G) protein sensitizes mice for pulmonary eosinophilia and because Th2 cells are central in the pathogenesis of asthma, plasma and peripheral blood mononuclear cells (PBMC) from donors with asthma and from healthy donors were evaluated for anti-G protein responses. A significant trend connecting severity of asthma with anti-G protein IgG1 and IgG2 titers was observed. The correlation between anti-F protein IgG3 titers and asthma severity approached significance. Peptide mapping studies revealed that more positive recall responses (interferon-gamma and interleukin-10 secretion) occurred after PBMC from donors with asthma were stimulated with peptides representing the nonglycosylated domain of G protein. The same peptides elicited more positive recall responses (proliferation and interferon-gamma secretion) in the PBMC of healthy donors. These data suggest that a mechanism may exist whereby adaptive immune responses against G protein contribute to wheezing.
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