IL17A and chronic obstructive pulmonary disease: Notably, ILC1-like NK cells were distinct from both NK cells and ILC1s, were functionally impaired and failed to control tumor growth and cytomegalovirus infection.233–235 Plasticity of ILC2s towards ILC1 was described in the lungs of patients suffering from chronic obstructive pulmonary disease (COPD) and was promoted by the cytokines IL-1, IL-12, and IL-18 and connected to the induction of T-bet.236 ILC2 conversion to IL-17-producing ILC3s was reported in mice and humans.