Journal
NATURE IMMUNOLOGY
Volume 17, Issue 1, Pages 48-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3312
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Funding
- National Institute of Allergy and Infectious Diseases
- National Institute of Arthritis, Musculoskeletal and Skin Diseases of the US National Institutes of Health [R01AI071043, R01AR064831, ES019964]
- National Institute of Environmental Health Sciences of the US National Institutes of Health [R01AI071043, R01AR064831, ES019964]
- Pennsylvania State University from the National Institutes of Health [T32 AI074551]
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Innate lymphoid cells (ILCs) 'preferentially' localize into barrier tissues, where they function in tissue protection but can also contribute to inflammatory diseases. The mechanisms that regulate the establishment of ILCs in barrier tissues are poorly understood. Here we found that under steady-state conditions, ILCs in skin-draining lymph nodes (sLNs) were continuously activated to acquire regulatory properties and high expression of the chemokine receptor CCR10 for localization into the skin. CCR10(+) ILCs promoted the homeostasis of skin-resident T cells and, reciprocally, their establishment in the skin required T cell-regulated homeostatic environments. CD207(+) dendritic cells expressing the transcription factor Foxn1 were required for the proper generation of CCR10(+) ILCs. These observations reveal mechanisms that underlie the specific programming and priming of skin-homing CCR10(+) ILCs in the sLNs.
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