Abstract
Innate lymphoid cells (ILCs), defined as a heterogeneous population of lymphocytes, have received much attention over recent years. They can be categorized into three subsets according to the expression profiles of transcription factors and differing levels of cytokine production. These cells are widely distributed in human organs and tissues, especially in mucosal tissue. The ILCs are involved in various physiological and pathological processes, including inflammation, worm expulsion, autoimmune disease and tumor progression, many of which have been investigated and clarified in recent studies. In the tumor microenvironment, group 2 innate lymphoid cells (ILC2s) have been proved to be able to either promote or inhibit tumor progression by producing different cytokines, recruiting diverse types of immune cells, expressing immunosuppressive molecules and by regulating the expression of certain inflammatory factors. This review summarizes recent research progress on the immunomodulatory functions of ILC2s in the tumor microenvironment and puts forward some perspectives for future study.
Highlights
Innate lymphoid cells (ILCs) are heterogeneous and highly conserved immune cell populations that occur during organism development
Based on the differential requirements for transcriptional factors and cytokine production, the non-cytotoxic ILCs can be further categorized into three groups: group 1 innate lymphoid cells (ILC1s); group 2 innate lymphoid cells (ILC2s); and group 3 innate lymphoid cells (ILC3s) [4, 5]
In response to IL-25, IL-33, and thymic stromal lymphopoietin (TSLP), which are mostly derived from epithelial cells, ILC2s are activated to produce the type 2 cytokines IL-4, IL-5, IL-9, IL-13, and other factors such as methionine-enkephalin (Met-Enk) and Amphiregulin (Areg), which suggests that ILC2s exhibit similar functions as CD4+ Th2 cells [5]
Summary
Innate lymphoid cells (ILCs) are heterogeneous and highly conserved immune cell populations that occur during organism development. The development of ILC2s depends on the transcriptional factors GATA-3 and retinoic acid receptor-related orphan receptor-α (RORα), mirroring the nature of Th2 cells.
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