期刊
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
卷 131, 期 1, 页码 128-U194出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2012.10.048
关键词
Peanut allergy; oral immunotherapy; IgE; IgG(4); peptide microarray; epitope; B cell; antibody affinity
资金
- National Institutes of Health (NIH)/National Institute of Allergy and Infectious Diseases (NIAID)
- American Lung Association
- Cephalon
- Foundation of the American College of Allergy, Asthma & Immunology (ACAAI)
- Mead Johnson
- NIH/NIAID
- National Peanut Board
- NIH
- Food Allergy & Anaphylaxis Network
- Abbott Nutrition International
- Kentucky Society for Allergy, Asthma Immunology
- New England Allergy Society
- ACAAI, Indiana University Medical School
- ACAAI, Riley Children's Hospital
- Spanish Society of Allergy & Clinical Immunology (Madrid, Spain)
- Oregon Allergy Asthma & Immunology Society
- NIAID
- Allertein Therapeutics and Food Allergy Initiative
- US Food and Drug Administration
- Journal of Allergy and Clinical Immunology
- NIH/HAI
- Dannon Co Probiotics
- Exploramed Development
- Intelliject
- McNeil Nutritionals
- Merck Co
- Novartis
- Nutricia
- Pfizer
- Portola Pharmaceuticals
- Schering-Plough
- Food Allergy Initiative
- National Peanut Board, Scientific Hospital Supplies (Nutricia North America)
- Wallace Research Foundation
- NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000030] Funding Source: NIH RePORTER
Background: Patients with peanut allergy have highly stable pathologic antibody repertoires to the immunodominant B-cell epitopes of the major peanut allergens Ara h 1 to 3. Objective: We used a peptide microarray technique to analyze the effect of treatment with peanut oral immunotherapy (OIT) on such repertoires. Methods: Measurements of total peanut-specific IgE (psIgE) and peanut-specific IgG(4) (psIgG(4)) were made with CAP-FEIA. We analyzed sera from 22 patients with OIT and 6 control subjects and measured serum specific IgE and IgG(4) binding to epitopes of Ara h 1 to 3 using a high-throughput peptide microarray technique. Antibody affinity was measured by using a competitive peptide microarray, as previously described. Results: At baseline, psIgE and psIgG(4) diversity was similar between patients and control subjects, and there was broad variation in epitope recognition. After a median of 41 months of OIT, polyclonal psIgG(4) levels increased from a median of 0.3 mu g/mL (interquartile range [25% to 75%], 0.1-0.43 mu g/mL) at baseline to 10.5 mu g/mL (interquartile range [25% to 75%], 3.95-45.48 mu g/mL; P < .0001) and included de novo specificities. psIgE levels were reduced from a median baseline of 85.45 kU(A)/L (23.05-101.0 kU(A)/L) to 7.75 kU(A)/L (2.58-30.55 kU(A)/L, P < .0001). Affinity was unaffected. Although the psIgE repertoire contracted in most OIT-treated patients, several subjects generated new IgE specificities, even as the total psIgE level decreased. Global epitope-specific shifts from IgE to IgG(4) binding occurred, including at an informative epitope of Ara h 2. Conclusion: OIT differentially alters Ara h 1 to 3 binding patterns. These changes are variable between patients, are not observed in control subjects, and include a progressive polyclonal increase in IgG(4) levels, with concurrent reduction in IgE amount and diversity. (J Allergy Clin Immunol 2013;131:128-34.)
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