Since IL-1β engages an IL-1 receptor on ILC3s and promotes their proliferation and IL-17A production14, these findings suggest that the smoking-induced sputum ILC3s and circulating memory-like CD4+CD45RO+ILC3 subset in asthma patients could be generated by smoke-damaged airway epithelial cells rather than circulating immune cells. Here, CD4 is linked to asthma.