Table 3.

Role of ILC in promoting or inhibiting CRC tumorigenesis.

Immune cell type	Prognosis		References
	Anti-tumor	Pro-tumor
NK cells	• High cytotoxicity • Recognition of cancer initiating cells	• Low number of infiltrating NK cells • Reduced level of activating receptors (e.g., NKp44, NKp30) • Increased expression of inhibitory receptors (e.g., TIGIT) • Low cytotoxicity	(61, 64, 65, 67)
ILC1	• Produce IFN-γ and cytotoxic molecules associated with anti-tumor immunity*	• Accumulate in inflamed tissue • IFN-γ promotes inflammation*	(58, 62)
ILC2	• High pre-operative serum IL-13 • IL-5 recruits eosinophils	• Local IL-13 promote tumor epithelial survival and proliferation. • Elevated IL-5 in ulcerative colitis, anti-IL-5 reduced eosinophils and colitis*	(76, 77, 81–83)
ILC3	• IL-17 recruits neutrophils to protect tissue barrier* • IL-22 promotes wound healing* and protects intestinal epithelial cells from genotoxic stress-induced DNA damage	• Overproduction of IL-17 promote inflammation and angiogenesis, and disrupt the intestinal epithelial barrier • Overproduction of IL-22 dysregulates epithelial proliferation	(96, 102, 103, 106, 108, 109, 112, 113)

^*Indirect evidence of involvement in CRC development.