ArticleNature communications2016
Epidermal Notch1 recruits RORγ(+) group 3 innate lymphoid cells to orchestrate normal skin repair.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 88 citations in OpenAlex.
- ILC3s as central regulators of mucosal homeostasis and disease pathogenesis (Review).International journal of molecular medicine · 2026Review
- Ziyuglycoside I promotes wound healing via GPR34-mediated activation of group 3 innate lymphoid cells.Chinese medicine · 2026Article
- Topographical variations in the skin barrier and their role in disease pathogenesis.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025Review
- Immune-Epithelial Cell Interactions during Epidermal Regeneration, Repair, and Inflammatory Diseases.International journal of stem cells · 2025Review
- Natural killer cells in skin: a unique opportunity to better characterize the many facets of an overlooked secondary lymphoid organ.Frontiers in immunology · 2025Review
- Immunological control of skin development: from homeostasis to developmental pathologies.Frontiers in immunology · 2025Review
- The Central Roles of Keratinocytes in Coordinating Skin Immunity.The Journal of investigative dermatology · 2024Review
- Commensal microbe regulation of skin cells in disease.Cell host & microbe · 2024Review
- Understanding Type 3 Innate Lymphoid Cells and Crosstalk with the Microbiota: A Skin Connection.International journal of molecular sciences · 2024Review
- Insights into the tissue repair features of MAIT cells.Frontiers in immunology · 2024Review
- The role of trained immunity in sepsis.Frontiers in immunology · 2024Review
- Scars.Nature reviews. Disease primers · 2023Review
- Protective and pathogenic functions of innate lymphoid cells in transplantation.Clinical and experimental immunology · 2023Review
- ILC3: a case of conflicted identity.Frontiers in immunology · 2023Review
- Autoimmune thyroid disease disrupts immune homeostasis in the endometrium of unexplained infertility women-a single-cell RNA transcriptome study during the implantation window.Frontiers in endocrinology · 2023Article
- Toward Understanding Wound Immunology for High-Fidelity Skin Regeneration.Cold Spring Harbor perspectives in biology · 2022Review
- Immune Cells in Cutaneous Wound Healing: A Review of Functional Data from Animal Models.International journal of molecular sciences · 2022Review
- Recruitment and activation of type 3 innate lymphoid cells promote antitumor immune responses.Nature immunology · 2022Article
- One Size Does Not Fit All: Diversifying Immune Function in the Skin.Journal of immunology (Baltimore, Md. : 1950) · 2022Review
- IL-17 and IL-22 are pivotal cytokines to delay wound healing ofFrontiers in immunology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 7 institutions in 3 countries.
Funding
Abstract
Notch has a well-defined role in controlling cell fate decisions in the embryo and the adult epidermis and immune systems, yet emerging evidence suggests Notch also directs non-cell-autonomous signalling in adult tissues. Here, we show that Notch1 works as a damage response signal. Epidermal Notch induces recruitment of immune cell subsets including RORγ(+) ILC3s into wounded dermis; RORγ(+) ILC3s are potent sources of IL17F in wounds and control immunological and epidermal cell responses. Mice deficient for RORγ(+) ILC3s heal wounds poorly resulting from delayed epidermal proliferation and macrophage recruitment in a CCL3-dependent process. Notch1 upregulates TNFα and the ILC3 recruitment chemokines CCL20 and CXCL13. TNFα, as a Notch1 effector, directs ILC3 localization and rates of wound healing. Altogether these findings suggest that Notch is a key stress/injury signal in skin epithelium driving innate immune cell recruitment and normal skin tissue repair.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.