Natural clinical tolerance to peanut in African patients is caused by poor allergenic activity of peanut IgE

作者：Wollmann E; Hamsten C; Sibanda E; Ochome M; Focke Tejkl M; Asarnoj A; Onell A; Lilja G; Gallerano D; Lupinek C; Thalhamer T; Weiss R; Thalhamer J; Wickman M; Valenta R; van Hage M^*

来源：Allergy, 2015, 70(6): 638-652.

DOI：10.1111/all.12592

• Africa
• allergen component
• allergy
• peanut
• tolerance

BackgroundIn Africa, peanuts are frequently consumed, but severe allergic reactions are rare. We investigated immunological patterns of clinical tolerance to peanut in peanut-sensitized but asymptomatic patients from central Africa compared to peanut-allergic and peanut-sensitized but asymptomatic patients from Sweden.
MethodsSera from allergic patients (n=54) from Zimbabwe sensitized to peanut but without allergic symptoms to peanut, and sera from peanut-allergic (n=25) and peanut-sensitized but asymptomatic (n=25) patients from Sweden were analyzed toward peanut allergen components (Ara h 1-3, 6, 8-9) and other allergen molecules from important allergen sources using microarray. IgE to Ara h 2 peptide epitopes was analyzed, and allergenic activity was assessed by basophil activation assay.
ResultsForty-six percent of the African and all peanut-allergic Swedish patients showed IgE toward one of the highly allergenic peanut allergens (Ara h 1-3, 6, 9). However, 48% of the African patients had IgE to cross-reactive carbohydrate determinants (CCDs) with low allergenic activity and 60% of the Swedish asymptomatic patients had IgE against the PR protein Ara h 8. IgG and IgG(4) specificities and levels could not discriminate between the African asymptomatic and Swedish peanut-allergic patients. Asymptomatic patients almost lacked IgE to Ara h 2 peptides, which were recognized by peanut-allergic patients. Peanut IgE from peanut asymptomatic patients showed poor allergenic activity compared with IgE from peanut-allergic patients.
ConclusionsNatural clinical tolerance to peanut in the African patients can be caused by IgE to low allergenic peanut components and by poor allergenic activity of peanut-specific IgE.

• 出版日期2015-6