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. Author manuscript; available in PMC: 2022 Feb 1.
Published in final edited form as: Ann Allergy Asthma Immunol. 2020 Sep 17;126(2):135–142. doi: 10.1016/j.anai.2020.09.011

Figure 2. Proposed mechanisms and targets of ILC2-mediated inflammation in AERD.

Figure 2.

In AERD, epithelial cytokines IL-33 and TSLP are increased in tissues and can stimulate ILC2s to produce IL-4, IL-5, IL-9, and IL-13. IL-13 promotes hyperresponsiveness and mucus production. IL-4 and IL-9 have autocrine effects on ILC2 activation in addition to IL-9 promoting mast cell accumulation. IL-5 stimulates eosinophil production and egress from bone marrow as well as contributing to recruitment and survival of eosinophils in tissues. In turn, eosinophils and mast cells produce PGD2 and CysLTs (that are elevated in AERD) which can activate ILC2s. PGD2 is also produced by ILC2s and has autocrine actions to promote cytokine production. ILC2s also highly express GATA-3 that is required for type 2 cytokine production. Approved and non-approved therapies that target various mediators in ILC2 driven inflammation are shown.