The expanding role of innate lymphoid cells and their T-cell counterparts in gastrointestinal cancers.

Innate lymphoid cells (ILCs) contribute to the regulation of gastrointestinal (GI) homeostasis. Over the past 15 years, there has been a large effort to dissect the mechanisms required for GI homeostasis, with a major focus on different immune cell populations and the cytokines that they produce. In contrast to T-helper (Th) cells, ILCs respond rapidly to cytokines in their microenvironment in the absence of specific antigens; however, once activated both cell populations have similar effector functions. Two effector cytokines produced by both ILC3 and Th17 cell populations, Interleukin (IL)-17 and IL-22, have taken center stage for their ability to signal directly to GI epithelial cells and promote epithelial cell survival. In this review, we outline our current understanding of ILCs in the GI tract, and focus on GI cancers associated with aberrant production of IL-17 and IL-22. We highlight evidence from both mouse and patient-based analyses and discuss how tumor cells may hijack the potential evolutionary redundancy of these two cell populations.