ArticleCell2016
Impaired Epidermal to Dendritic T Cell Signaling Slows Wound Repair in Aged Skin.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
163 citing papers in PubMed, 251 citations in OpenAlex.
- Within-patient randomised clinical trial exploring the development of microskin implantation in the treatment of pressure ulcers.International wound journal · 2023Trial
- Skin Aging: From Molecular Mechanisms to Therapeutic and Technological Innovations.Journal of cellular and molecular medicine · 2026Review
- Distinct postnatal trajectories of mouse dendritic epidermal T cells and Langerhans cells independent of microbiota.Science advances · 2026Article
- Mechanisms and Clinical Manifestations of Age-Related Impairment in Wound Healing.International wound journal · 2026Review
- The In Vitro Wound-Scratch Assay: Applications, Technical Advances, and Limitations in Wound Healing Research.International wound journal · 2026Review
- Transient immunostimulation with LPS promotes tissue repair in aged skin.Immunity & ageing : I & A · 2026Article
- γδ T cell-stromal networks modulate matrix composition and vascularity in foreign body response.Nature communications · 2026Article
- Ketogenic diet synergistic reprogramming of both host and microbiome promotes tissue regeneration.bioRxiv : the preprint server for biology · 2026Article
- Chemical anchoring of immunotherapeutic drugs within senescent tumor cells overcomes senescence-driven immunotherapy resistance.Nature communications · 2026Article
- Tick Extracellular Vesicles Alter Epidermal Keratinocyte Function.The Journal of investigative dermatology · 2026Article
- Distinctive DNA sequence features define epigenetic longevity of inflammatory memory.Science (New York, N.Y.) · 2026Article
- Stromal-Derived Factor-1 (SDF-1/CXCL12) and Skin Wound Healing Research at the Intersection Between Regenerative Biology and Medicine.International journal of molecular sciences · 2026Review
- Overexpression of Neuropeptide Y Leads to Progressive, Cutaneous Inflammatory Fibrotic Responses in Mouse Skin.The Journal of investigative dermatology · 2026Article
- Mosaic partial epidermal reprogramming remodels neighbors and niches to refine skin homeostasis and repair.Nature communications · 2026Article
- Beyond scarring: immune-epithelial crosstalk in wound-induced hair follicle neogenesis.Frontiers in immunology · 2026Review
- Dysregulated NAMPT signaling underlines the immune-suppressive microenvironment in venous leg ulcers.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Single Cell Sequencing Identifies Distinct Cellular Alterations in Impaired Aged and Diabetic Wounds.Aging cell · 2025Article
- How stem cells respond to infection, inflammation and ageing.Nature reviews. Immunology · 2025Review
- Intrinsic changes in cell differentiation and identity drive impaired wound healing in aged female murine skin.Biogerontology · 2025Article
- Injured bone-triggered osteokines secretion promotes diabetic wound healing.Bone research · 2025Article
103 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Aged skin heals wounds poorly, increasing susceptibility to infections. Restoring homeostasis after wounding requires the coordinated actions of epidermal and immune cells. Here we find that both intrinsic defects and communication with immune cells are impaired in aged keratinocytes, diminishing their efficiency in restoring the skin barrier after wounding. At the wound-edge, aged keratinocytes display reduced proliferation and migration. They also exhibit a dampened ability to transcriptionally activate epithelial-immune crosstalk regulators, including a failure to properly activate/maintain dendritic epithelial T cells (DETCs), which promote re-epithelialization following injury. Probing mechanism, we find that aged keratinocytes near the wound edge don't efficiently upregulate Skints or activate STAT3. Notably, when epidermal Stat3, Skints, or DETCs are silenced in young skin, re-epithelialization following wounding is perturbed. These findings underscore epithelial-immune crosstalk perturbations in general, and Skints in particular, as critical mediators in the age-related decline in wound-repair.
Indexed as
Identifiers
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.