Abstract
Tissue-resident immune cells reside in distinct niches across organs, where they contribute to tissue homeostasis and rapidly respond to perturbations in the local microenvironment. Innate lymphoid cells (ILCs) are a family of innate immune cells that regulate immune and tissue homeostasis. Across anatomical locations throughout the body, ILCs adopt tissue-specific fates, differing from circulating ILC populations. Adaptations of ILCs to microenvironmental changes have been documented in several inflammatory contexts, including obesity, asthma, and inflammatory bowel disease. While our understanding of ILC functions within tissues have predominantly been based on mouse studies, development of advanced single cell platforms to study tissue-resident ILCs in humans and emerging patient-based data is providing new insights into this lymphocyte family. Within this review, we discuss current concepts of ILC fate and function, exploring tissue-specific functions of ILCs and their contribution to health and disease across organ systems.
Highlights
Innate lymphoid cells (ILCs) orchestrate immune responses to signals such as cytokines, alarmins, neuropeptides and hormones, interacting with hematopoietic and non-hematopoietic cells alike
GATA3 and an upregulation of T-BET, increasing IFN-g release while dampening IL-4 and IL-13 production [89, 106]. These results collectively demonstrate that persistent lung inflammation and exposure to smoke leads to changes in the local ILC composition and function (Figure 4D)
A better understanding of homologies and analogies in their surface receptor expression and function are needed to inform conserved mechanisms underlying responses to infections, inflammation and malignancies. This will be of particular interest to enhance our understanding NK cell biology, where receptors regulating NK cells responses differ between mouse and human, but different receptors often perform similar function
Summary
Innate lymphoid cells (ILCs) orchestrate immune responses to signals such as cytokines, alarmins, neuropeptides and hormones, interacting with hematopoietic and non-hematopoietic cells alike. ILC2s have conflicting roles in influenza infection response, promoting airway hyperreactivity in an IL-13-dependent manner while supporting epithelial cell integrity and tissue repair via the secretion of AREG following viral infections [85, 86].
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