Fig. 1

Innate lymphoid cell (ILC) effector functions. A NK cells are characterized by the expression of the transcription factors eomesodermin (Eomes) and T-bet (encoded by TBX21). Activated NK cells produce type I cytokines, including the signature cytokine IFNγ. NK cells recognize target cells via a combination of activation and inhibitory receptors and subsequently kill the target cells in a perforin/granzyme-, FAS-, or TRAIL-dependent manner. NK cells also recognize and kill antibody-coated target cells through Fc receptors (FcRs), resulting in antibody-mediated cytotoxicity (ADCC). NK cells have the capacity to kill activated virus-specific CD4+ T cells via TRAIL- and perforin-dependent mechanisms, but their receptor‒ligand interactions have not yet been elucidated. In response to activation, NK cells expand and peak around Day 7, after which the population contracts to form a long-lived adaptive compartment. B ILC1s are characterized by the expression of the transcription factors Hobit (encoded by ZNF683) and T-bet. ILC1s produce type I cytokines, including IFNγ and TNFα. ILC1s expand, contract, and form an adaptive compartment. Based on depletion studies, ILC1s have been implicated in directly recognizing and killing virus-infected cells in a TRAIL-dependent manner. C ILC2s are characterized by high expression of the transcription factor GATA3 and produce type II cytokines. ILC2s can produce amphiregulin (AREG), which is involved in tissue repair. Within the tumor microenvironment, ILC2s can express the checkpoint programmed cell death 1 (PD1) and modulate tumor-specific T-cell responses. D ILC3s express the transcription factor RAR-related orphan receptor γT (RORγT) and produce type III cytokines, including IL-17 and IL-22. IL-22 produced by ILC3s stimulates the production of antimicrobial peptides and the expansion of intestinal stem cells (ISCs) to maintain barrier function. E Lymphoid tissue inducer (LTi) cells are also characterized by the expression of the transcription factor RORγT and the production of type III cytokines. LTi induces the formation of secondary lymphoid organs (SLOs) in a manner dependent on lymphotoxin and receptor activator of nuclear factor kappa B (RANK)