The lipid interaction capacity of Sin a 2 and Ara h 1, major mustard and peanut allergens of the cupin superfamily, endorses allergenicity.

Sin a 2 (11S globulin) and Ara h 1 (7S globulin) are major allergensfrom yellow mustard seedsand peanut, respectively. The ability of these two allergensto interact with lipidcomponents remains unknown.To study the capacity of Sin a 2 and Ara h 1 to interact with lipidcomponents and the potential effects of such interaction in their allergeniccapacity.Spectroscopic and SDS-PAGE binding assays of Sin a 2 and Ara h 1 with different phospholipid vesicles and gastrointestinal and endolysosomal digestions in the presence or absence of lipidswere performed. The capacity of human monocyte-derived dendritic cells (hmoDCs) to capture food allergensin the presence or absence of lipids, the induced cytokine signature, and the effect of allergensand lipidsto regulate TLR2-L-induced NF-kB/AP-1 activation in THP1 cells were analyzed.Sin a 2 and Ara h 1 bind phosphatidylglycerol(PG) acid but not phosphatidylcholine (PC) vesicles in a pH-dependent manner. The interaction of these two allergenswith lipidcomponents confers resistance to gastrointestinal digestion, reduces their uptake by hmoDCs, and enhances their stability to microsomal degradation. Mustard and peanut lipidsfavor a proinflammatory environment by increasing the IL-4/IL-10 ratio and IL-1β production by hmoDCs. The presence of mustard lipidsand PG vesicles inhibits TLR2-L-induced NF-kB/AP-1 activation in THP1 cells.Sin a 2 and Ara h 1 interact with lipidcomponents, which might well contribute to explain the potent allergeniccapacity of these two clinically relevant allergensbelonging to the cupin superfamily.