Abstract
Innate lymphoid cells (ILCs) are a group of immune cells that are important for defense against pathogens, tissue repair, and lymphoid organogenesis. They share similar characteristics with various subsets of helper T cells but lack specific antigen receptors. Interleukin-7 (IL-7) and thymic stromal lymphopoietin (TSLP) are cytokines that engage the IL-7Rα and have major roles in dictating the fate of ILCs. Recent advances in the field have revealed transcriptional programs associated with ILC development and function. In this article, we will review recent studies of the role of IL-7 and TSLP in ILC development and function during infection and inflammation.
Highlights
Innate lymphoid cells (ILCs) are a recently discovered subset of immune cells critical for the development of innate immunity against external pathogens, facilitating tissue repair, and mediating inflammation at multiple mucosal sites [1]
In addition to inducing GATA3 in ILC2s, a recent studies have found STAT5 to be a major regulator of ILC homeostasis by regulating multiple networks ranging from survival factors such as Bcl-2 and transcription factors such as T-bet, RORγt, and Sall3 which each play a role in the function and differentiation of various ILC subsets [70, 71] (Figure 2)
IL-7 and thymic stromal lymphopoietin (TSLP) signal through IL-7Rα and play multiple roles in determining the fate of ILCs and T cells
Summary
Innate lymphoid cells (ILCs) are a recently discovered subset of immune cells critical for the development of innate immunity against external pathogens, facilitating tissue repair, and mediating inflammation at multiple mucosal sites [1]. Group 3 ILCs (ILC3s) are RORγt-dependent, like Th17 cells, and consist of a major subset that produces IL-17 and IL-22 in response to IL-23 and are critical for intestinal immunity against pathogens [1, 53]. Another subset of ILCs are the Lymphoid Tissue inducer cells (LTi), which are RORγt-dependent group 3 ILCs, and are considered important for the development of secondary lymphoid organs [54].
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