Human subjects without peanut allergy demonstrate T cell–dependent, TH2-biased, peanut-specific cytokine and chemokine responses independent of TH1 expression - 16/08/11
, Wesley Burks, MD d, Kent T. HayGlass, PhD a, b, ⁎ 
for the Canadian Institutes of Health Research National Training Program in Allergy and Asthma Research
Reprint requests: Kent T. HayGlass, PhD, Canada Research Chair in Immune Regulation, Department of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada R3E 0W3.Winnipeg, Manitoba, Canada, Little Rock, Ark, and Durham, NC
Abstract |
Background |
Peanut allergy is a major cause of anaphylaxis. Regulation of immune responses to peanut allergen, particularly why sensitization does not usually progress to allergic reactions, is not well investigated. Most studies focus exclusively on serologic responses and individuals with peanut allergy.
Objective |
We sought to determine the existence, prevalence, and nature of peanut-specific, T cell–dependent cytokine and chemokine responses of adults who eat peanut without having symptoms.
Methods |
We developed systems to examine specific immunity in peanut-tolerant individuals who had (1) negative histories and negative peanut skin test responses, (2) negative histories and positive peanut skin test responses, and (3) clinically apparent peanut allergy. After primary culture of PBMCs restimulated with whole peanut extract, we quantified responses characteristic of TH1 (IFN-γ and CXCL10) and TH2-like immunity (IL-5, IL-13, CCL17, and CCL22) using ultrasensitive ELISAs. Antigen-presenting cell costimulatory requirements (CD4, HLA-DR, CD80/86, and cytotoxic T lymphocyte–associated antigen 4 [CTLA4] Ig) were determined.
Results |
T cell–dependent, peanut-specific IL-5, IL-13, and CCL22 were common in peanut-tolerant individuals, regardless of whether they had positive or negative skin test responses. These were blocked by anti-CD4 and were dependent on CD28/CD86 costimulation. None of the 70 individuals studied had demonstrable IFN-γ or CXCL10 responses to peanut. All demonstrated TH1 and TH2 responses to the ubiquitous recall antigen streptokinase.
Conclusions |
Qualitatively similar and quantitatively increasing peanut-specific TH2 responses in the consistent absence of putatively protective TH1 immunity were found in both peanut-tolerant individuals and those with peanut allergy.
Clinical implications |
The continuum of responses between individuals with negative and individuals with positive skin test results, rather than TH1 versus TH2 bias, might be important in peanut allergy.
Le texte complet de cet article est disponible en PDF.Key words : Food allergy, peanut allergy, anaphylaxis, T cell, cytokine, chemokine, costimulation
Abbreviations used : CTLA4, PMA, SPT, WPE
Plan
| Supported by the Canadian Institutes of Health Research, Canada Research Chairs program, Manitoba Institute of Child Health, and the Canadian Asthma Allergy and Immunology Foundation/Anaphylaxis Canada Partnership. Disclosure of potential conflict of interest: W. Burks has received grant support from the National Peanut Board and owns stock in Seer, Inc. The rest of the authors have declared that they have no conflict of interest. |
Vol 118 - N° 4
P. 905-914 - octobre 2006 Retour au numéro
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