Abstract Allergic reactions to peanut (Arachis hypogaea, Arah) are caused by immunoglobulin E (IgE)-mediated sensitizations to various proteins.  e stability and relative proportion of these proteins in peanut determine the risk of hazardous reactions. Hazardous sensitization to seed storage proteins [S2 albumins (Ara h 2, 6 and 7) > other seed storage proteins
(Ara 1 and 3) > oleosins (Ara h 10 and 11)] are distinct from sensitizations to lipid transfer protein (Ara h 9) with moderate risk or cross-sensitizations to Bet v 1-homologous PR-10 protein (Ara h 8) and to pro lin (Ara h 5) with low risk. A speci c IgE test, e.g. to Ara h 2 in the case of suspected systemic reaction, or where this should be ruled out, can facilitate easier risk assessment. Results, however, are only relevant in the presence of corresponding clinical
symptoms. IgE sensitization to peanut extract without hazardous reactions is o en caused in this
part of the world by Bet v 1-related cross reactions (in birch pollen allergy su erers), cross-reactive carbohydrate determinants (CCD) or pro lin sensitizations. In the case of doubt, clinical relevance can only be established by means of oral challenge, particularly since not all peanut allergens (e. g., oleosins) are available as yet for diagnostic purposes