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ILC plasticity in response to lung infections. In steady state lungs contain tissue-resident immature IL-18R+TCF1+ GATA3lo ILCs which can differentiate into ILC2s. Respiratory infections facilitate maturation of IL-18R+ ILCs. Type 1 inflammatory cytokines (IL-12+IL-1β) drive ILC2→ILC1 plasticity by downregulating GATA3 and upregulating T-bet. T-bet induces production of IFNγ by ILC1s. Additionally, IL-22 and IL-17 produced by ILC3s support protective responses via iBALT maintenance.
