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. Author manuscript; available in PMC: 2019 Jul 21.
Published in final edited form as: Mucosal Immunol. 2019 Jan 21;12(3):679–690. doi: 10.1038/s41385-019-0134-8

Figure 7.

Figure 7.

Schematic showing putative initiating (CysLT2R-dependent) and downstream (CysLT1R and CysLT3R) dependent effects of cysLTs in driving the mechanism responsible for reactions to aspirin. Platelet CysLT2R is essential to initiate HMGB1/RAGE signaling that permits platelet activation and conjugation to granulocytes. Platelets adherent to granulocytes and activated via CysLT2R/HMGB1/RAGE provide a pool of IL-33 that drives MC activation and a secondary surge of cysLTs to act at cognate receptors, and also activates ILC2s to promote additional type 2 immunopathology.