Inhibition of allergen-IgE binding to B cells by IgG antibodies after grass pollen immunotherapy
- PMID: 14610480
- DOI: 10.1016/s0091-6749(03)02022-0
Inhibition of allergen-IgE binding to B cells by IgG antibodies after grass pollen immunotherapy
Abstract
Background: Among atopic individuals, levels of allergen-specific IgG antibodies have been inversely associated with the degree of allergen sensitization. Additionally, allergen-specific IgG antibodies are markedly increased by allergen injection immunotherapy. These observations have led to proposals that allergen-specific IgG antibodies might have protective properties in atopic individuals.
Objective: We hypothesized that after grass pollen immunotherapy, these antibodies disrupt IgE-dependent allergen processing by antigen-presenting cells.
Methods: We have developed a novel flow cytometric assay based on detection of allergen-IgE binding to the low-affinity IgE receptor on B cells to examine the blocking effects of sera collected from 18 patients who participated in a double-blind, controlled trial of grass pollen immunotherapy for 1 year.
Results: In all 10 patients who received active therapy, there was induction of activity that inhibited allergen-IgE binding to B cells (P =.02, vs placebo subjects), as well as subsequent allergen presentation to T cells. This activity copurified with IgG and was allergen specific, because sera taken from patients treated with grass pollen immunotherapy but who were also birch pollen sensitive did not inhibit IgE-birch pollen allergen binding to B cells.
Conclusion: We conclude that allergen-specific IgG antibodies induced by immunotherapy can disrupt formation of allergen-IgE complexes that bind to antigen-presenting cells and facilitate allergen presentation.
Comment in
-
Anti-idiotype antibodies could explain inhibition of allergen-IgE binding to B cells after grass pollen immunotherapy.J Allergy Clin Immunol. 2004 Jun;113(6):1225; author reply 1225-6. doi: 10.1016/j.jaci.2004.01.776. J Allergy Clin Immunol. 2004. PMID: 15214366 No abstract available.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
