165 : Critical regulation of type 2 innate lymphoid cells by mast cells during allergic airway inflammation

Mast cells and basophils mediate tissue inflammation during allergy and anaphylaxis by secreting granules and cytokines; however, their role in the development of Th2 cells and type 2 innate lymphoid cells (ILC2) is not fully understood. Bas-TRECK and Mas-TRECK mice have been recently described to express diphtheria toxin receptor exclusively on basophils, or on both basophils and mast cells, respectively. Here, by using these genetic tools, we show that depletion of basophil minimally affected the size of pulmonary Th2 cells in response to fungal protease allergens, whereas additional depletion of mast cells almost completely abolished pulmonary Th2 responses as well as infiltration of inflammatory cells into airway. Of note, diphtheria toxin-treated Mas-TRECK mice exhibited a significant decrease in the frequency and number of Lin − CD45 + CD127 + IL-13-producing ILC2 in the lung compared to wild-type and Bas-TRECK mice that received same treatment. Moreover, lungs of the toxin-treated Mas-TRECK mice showed significantly decreased expression of Il33 transcript than those of wild-type. Our findings together unveil a critical contribution of mast cells rather than basophils to the induction of ILC2 as well as Th2 cells in the airway in response to fungal allergen in vivo.