L activity. Conclusions: The massive aggregates of gliadins that could happen for the duration of bread-making displayed a decreased allergenicity in vitro in comparison to native gliadins. This could be associated for the capacity of some individuals to achieve hypo-responsiveness to wheat for the duration of oral immunotherapy protocols performed with bread or other heated wheat-based items. P13 Scavenger receptor class a mediates uptake of Ara H 1, a significant peanut allergen, by human M2 RW22164 (acetate);RWJ22164 (acetate) Autophagy macrophages Maren Krause1, Peter Crauwels2, Martin Globisch3, Thomas Henle3, Ger Van Zandbergen2, Stefan Vieths1, Stephan Scheurer1, Masako Toda1 1 VPr1 Study Group “Molecular Allergology”, PaulEhrlichInstitut, Langen, Germany; 2Division of Immunology, PaulEhrlichInstitut, Langen, Germany; 3Institute of Meals Chemistry, Technical University Dresden, Dresden, Germany Correspondence: Maren Krause [email protected] Clinical Translational Allergy (CTA) 2018, 8(Suppl 1):P13 Background: Ara h 1 potentially contributes to peanut-induced anaphylactic reactions as a major peanut allergen. Dendritic cell-specific ICAM-grabbing nonintegrin (DC-SIGN) is described as receptor for Ara h 1 to activate human dendritic cells (Shreffler et al., J. Immulol. 2006), whereas Ara h 1-mediated activation of macrophages is less investigated. Considering that evidence has accumulated that not simply dendritic cells but additionally macrophages play a vital part in improvement and upkeep of meals allergy, we aimed to investigate interaction of Ara h 1 with human main macrophages. Strategies: M1 and M2 macrophages have been generated by culturing peripheral blood derived monocytes from healthy donors in the presence of rGM-CSF and rM-CSF for 6-8 days, respectively. Ara h 1 was isolated from unroasted peanut. Levels of Ara h 1 uptake and receptor expression by macrophages have been assessed by flow cytometry. The levels of secreted cytokines by Ara h 1-stimulated cells were assessed by ELISA. Interaction of Ara h 1 with receptors expressed around the cell surface of macrophages was investigated utilizing inhibitors of putative cell surface receptors and modest interfering RNA.Clin Transl Allergy 2018, eight(Suppl 1):Web page six ofResults: Upon stimulation with Ara h 1, M1 macrophages created larger levels of pro-inflammatory cytokines IL-6 and TNF- than M2 macrophages. In contrast, M2 macrophages internalized Ara h 1 to a higher extent than M1 macrophages. M1 macrophage expressed DC-SIGN and SR-A only at marginal levels, whereas M2 macrophages expressed both receptors at considerable levels. Compact interfering RNA knockdown of DC-SIGN in M1 and M2 macrophages did not suppress the uptake of Ara h 1 by the cells. Nevertheless, inhibitors for scavenger receptor class A (SR-A), e.g. polyinosinic acid and acetylated low density lipoprotein, suppressed M2 macrophage-mediated, but not M1 macrophage-mediated uptake of Ara h 1. Conclusions: In this study, we demonstrated that DC-SIGN is most likely to not be a significant receptor involved in the interaction of Ara h 1 by human primary macrophages. SR-A is demonstrated to partly mediate the interaction of Ara h 1 with M2 macrophages, which play an active role inside the pathogenesis of allergy. Further research are Flumioxazin Data Sheet necessary to get a deeper understanding of the interaction in between Ara h 1 and M2 macrophages and to unravel the mechanism underlying the intrinsic allergenicity. P14 Genetic variation influences the influence of PGE2 on allergic responses in murine mast cells Shruti Rastogi, Maria Nassiri, Magda Babina, Margitta Worm AllergyCen.