Relevance for Helper ILCs in SARS-CoV-2 Infection
No studies, to date, have reported ILC1, ILC2, or ILC3 functions in SARS-CoV-2 infection. All three subsets are present in healthy lung (De Grove et al., 2016, Yudanin et al., 2019). ILC2s are essential for the improvement of lung function following influenza infection in mice through amphiregulin-mediated restoration of the airway epithelium and oxygen saturation (Monticelli et al., 2011). However, ILC2s also produce IL-13, contributing to the recruitment of macrophages to the lung and influenza-induced airway hyperreactivity (Chang et al., 2011). Indeed, ILCs are involved in the polarization of alveolar macrophages, either toward a M1-like phenotype (ILC1 and ILC3) or a M2-like phenotype (ILC2) (Kim et al., 2019). Given the increased IL-13 concentrations (Huang et al., 2020b) and the dysregulation of the macrophage compartment observed in COVID-19 patients, the role played by ILCs in SARS-CoV-2 infection warrants further investigation.