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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 1. Recruitment of ILC2s to respiratory mucosa in AERD.

Figure 1.

In patients with AERD challenged with COX-1 inhibitors, CRTH2+ ILC2s are reduced in the blood and accumulate in the nasal mucosa concomitantly with increased urinary prostaglandin D2 metabolites. This suggests that ILC2s that express CRTH2 (receptor for PGD2) may traffic into respiratory tissues from the bone marrow during COX-1 inhibition in AERD patients. Whether ILC2 recruitment occurs over time in the absence of COX-1 inhibitor challenge (‘steady state AERD’) is not known. Once in tissues, type 2 cytokine production by ILC2s and other cell types can promote tissue eosinophilia, mast cell activation, mucus hypersecretion, and airway hyperresponsiveness.