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Roberts, L. B., Kelly, A. M., & Hepworth, M. R. (2025). There’s no place like home: How local tissue microenvironments shape the function of innate lymphoid cells. Society for Mucosal Immunity, 18(2), 279–289. 
Added by: Dr. Enrique Feoli (12/07/2025, 19:30)   Last edited by: Dr. Enrique Feoli (12/07/2025, 19:42)
Resource type: Journal Article
DOI: 10.1016/j.mucimm.2025.01.012
ID no. (ISBN etc.): 1935-3456
BibTeX citation key: Roberts2025
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Categories: BioAcyl Corp
Keywords: Extracellular Matrix, Immunoregulation, Innate Lymphoid Cells, Metabolism, tissue microenvironment
Creators: Hepworth, Kelly, Roberts
Collection: Society for Mucosal Immunity
Views: 6/25
Abstract
Innate lymphoid cells (ILC) have emerged as critical immune effectors with key roles in orchestrating the wider immune response. While ILC are relatively rare cells they are found enriched within discrete microenvironments, predominantly within barrier tissues. An emerging body of evidence implicates complex and multi-layered interactions between cell types, tissue structure and the external environment as key determinants of ILC function within these niches. In this review we will discuss the specific components that constitute ILC-associated microenvironments and consider how they act to determine health and disease. The development of holistic, integrated models of ILC function within complex tissue environments will inform new understanding of the contextual cues and mechanisms that determine the protective versus disease-causing roles of this immune cell family.
  
Notes

Interactions of Innate Lymphoid Cells with the extracellular matrix. (A). ILC reside in microenvironments rich in extracellular matrix (ECM). Within the lungs ILC2 predominantly associate with collagen-rich regions including the perivascular adventitial cuff and peribronchial regions surrounding blood vessels and airways. Within these sites, ILC2 interact with collagen-producing cell types including adventitial stromal cells which are also rich sources of ILC2- activating cues, including interleukin (IL)–33 and thymic stromal lymphopoietin (TSLP). (B). Interactions with ECM components including collagens can be perceived by ILC via expression of ECM-sensing receptors. Furthermore, ECM components may drive cytoskeletal remodelling which facilitates promotion of migratory activities of ILC. ILC also have the capacity for mechanosensing and respond to alterations to mechanical cues through Piezo-1 ion channels to shape ILC behaviours. (C). ILCs may also provide instructive cues that remodel and shape the ECM composition of their tissue niches. For example, following tissue damage or disease-associated repair processes, ILC2 production of effector cytokines and proteins including IL-13 and amphiregulin (AREG) can act to promote ECM remodelling of their surrounding niches, inducing expansion of stromal cell populations responsible for production and deposition of ECM components including collagens and hyaluronan/hyaluronic acid (HA).


  
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