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Different groups of Innate lymphoid cells have ability to influence tumorigenesis in several ways.

ILC1 are the major population of ILC with anti-tumorigenic potential. The best explored ILC1 are NK cells. Their function is regulated by signals from stimulatory and inhibitory receptors. NK cells have ability to recognize missing MHC class I on tumor cell. In this way, they act in a complementary manner with the cytotoxic T cells that recognize and kill tumor cells which present a foreign antigen on MHC class I. NK cells express a number of cell surface activating NK cell receptors with specificity for stress induced ligands overexpressed on tumor cell. In humans, receptor NKG2D recognize ULBP1-6 and MICA, MICB, RAET1E whereas in mice it binds RAE1 family molecules, H60 family molecules and MULT1 protein. Another family of activating NK cell receptors are NCRs (natural cytotoxicity receptors), DNAM1 (DNAX Accessory Molecule-1 CD266) and CD16 (mediate ADCC after binding of tumor specific antibody on tumor antigen). ILC1 influence tumor microenvironment by production of several cytokines like IFNg and TNFa which at the beginning of immune response polarize other immune cells into inflammatory phenotype, e.g. M1 macrophages. ILC1 also recruit DC and cytotoxic T cells. On the other hand IFN g and TNF a play important role in induction of immunosupressive phenotype of immune cells or MDSC, production of anti-inflammatory cytokines and formation of metastases.

Other ILC populatins also influence tumor microenvironment. ILC2 produce cytokines that promote anti-inflammatory immune response e.g. IL-13, IL-4, Amphiregulin. However in some settings ILC2 produce IL-5 and promote cytotoxic response of eosinophils and antitumor response and metastasis suppression.

ILC3 are involved in inflammation-related tumorigenesis by production of IL-17, IL-22, IL-23 cytokines. This microenvironment leads to tumor development and progression and contribute for better survival of cancer cells.