Cited by 49IL-33, ST2, and ILC PathwaysT-cell and B-cell ImmunologyDermatology and Skin Diseases

Selective programming of CCR10(+) innate lymphoid cells in skin-draining lymph nodes for cutaneous homeostatic regulation

Open access
Yang, Jie, Hu, Shaomin, Zhao, Luming, Kaplan, Daniel H, Perdew, Gary H, Xiong, Na·2016·Nature Immunology

Abstract

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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Crossref · 10.1038/ni.3312

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  • FTY720 blocks migration of T cells and ILCs from circulation into the skin by impairing S1PR1-mediated signals.

    “FTY720 blocks the migration of T cells and ILCs from circulation into the skin by impairing sphingosine-1-phosphate receptor 1 (S1PR1)-mediated signals.18,19”

    From Skin-resident T cells play an important role in controlling skin colonization of Candidozyma (Candida) auris (2026) · cites this paper as [19]

    In Results (‘Predominant migration of CCR10+MHCII+ ILCs of sLN into the skin’; page unavailable), FTY720-treated mice had fewer CCR10+ ILCs and T cells in skin and more in skin-draining lymph nodes. This supports reduced skin presence of those cells, but the paper describes input from lymph nodes rather than directly demonstrating blocked migration from circulation, and it does not establish an S1PR1-mediated mechanism. (LLM, conf=0.88)

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Cited by

Sorted by citations

Authors
Yang, J., Hu, S., Zhao, L., Kaplan, D. H., Perdew, G. H., & Xiong, N.
Affiliations
  • Pennsylvania State University (US)
  • University of Minnesota (US)
Corresponding author
Xiong, Na
Venue
Nature Immunology
Published
2015-11-02
Volume
17
Issue
1
Pages
48-56
ISSN
  • 1529-2908 (ISSN-L)
  • 1529-2916
OpenAlex
W2214891315
Cited by
49
References
2
Citations by year
2026: 3 · 2025: 5 · 2024: 1 · 2023: 3 · 2022: 6 · 2021: 6 · 2020: 10 · 2019: 4 · 2018: 4 · 2017: 4 · 2016: 3
FWCI
1.81
Type
journal article
Language
en
Open access
Locations
  • Nature Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute of Allergy and Infectious Diseases (R01AI071043, T32AI074551)
  • National Institute of Environmental Health Sciences (R01ES019964, ES019964)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR064831)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
Keywords
innate lymphoid cells, CCR10, skin-draining lymph nodes, skin homeostasis, Foxn1, skin-resident T cells, barrier tissues, chemokine receptor signaling
MeSH terms
Animals, Flow Cytometry, Homeostasis, Immunity, Innate, Lymph Nodes, Lymphocytes, Mice, Inbred C57BL, Skin, Mice, Knockout, Adoptive Transfer, Mice, Receptors, CCR10

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