ArticleProceedings of the National Academy of Sciences of the United States of America2012
Autocrine/paracrine TGF-β1 inhibits Langerhans cell migration.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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
73 citing papers in PubMed, 110 citations in OpenAlex.
- Dual Lineages of Langerhans Cells Cooperate to Restore the Immune Barrier after Skin Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Dual lineages of Langerhans cells cooperate to restore the immune barrier after skin injury.bioRxiv : the preprint server for biology · 2026Article
- Cutaneous Dendritic Cells: Structure, Function and Immune Role.Biomedicines · 2026Review
- Epidermal maintenance of Langerhans cells relies on autophagy-regulated lipid metabolism.The Journal of cell biology · 2025Article
- Unraveling cutaneous histiocytosis: insights into histology, pathogenesis, diagnosis, and treatment pitfalls.Frontiers in medicine · 2025Review
- LangerinClinical, cosmetic and investigational dermatology · 2025Review
- Vitamin K supports TGF-β1 dependedFrontiers in immunology · 2025Article
- Monocytes give rise to Langerhans cells that preferentially migrate to lymph nodes at steady state.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Cell shape sensing licenses dendritic cells for homeostatic migration to lymph nodes.Nature immunology · 2024Article
- Dendritic Cells: A Bridge between Tolerance Induction and Cancer Development in Transplantation Setting.Biomedicines · 2024Review
- Immunomodulatory potential of primary cilia in the skin.Frontiers in immunology · 2024Review
- 3D sheep rumen epithelial structures driven from single cells in vitro.Veterinary research · 2023Article
- Metabolic adaption of mucosal macrophages: Is metabolism a driver of persistence across tissues?Mucosal immunology · 2023Review
- Intricacies of TGF-β signaling in Treg and Th17 cell biology.Cellular & molecular immunology · 2023Review
- Article
- T cell and bacterial microbiota interaction at intestinal and skin epithelial interfaces.Discovery immunology · 2023Review
- Langerhans cells are essential components of the angiogenic niche during murine skin repair.Developmental cell · 2022Article
- BMPR1a Is Required for the Optimal TGFβ1-Dependent CD207The Journal of investigative dermatology · 2022Article
- Review
- Loricrin at the Boundary between Inside and Outside.Biomolecules · 2022Review
13 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
6 authors at 3 institutions in 1 country.
Funding
Abstract
Langerhans cells (LCs) are skin-resident dendritic cells (DC) located in the epidermis that migrate to skin-draining lymph nodes during the steady state and in response to inflammatory stimuli. TGF-β1 is a critical immune regulator that is highly expressed by LCs. The ability to test the functional importance of LC-derived TGF-β1 is complicated by the requirement of TGF-β1 for LC development and by the absence of LCs in mice with an LC-specific ablation of TGF-β1 or its receptor. To overcome these problems, we have engineered transgenic huLangerin-CreER(T2) mice that allow for inducible LC-specific excision. Highly efficient and LC-specific expression was confirmed in mice bred onto a YFP Cre reporter strain. We next generated huLangerin-CreER(T2) × TGF-βRII(fl) and huLangerin-CreER(T2) × TGF-β1(fl) mice. Excision of the TGFβRII or TGFβ1 genes induced mass migration of LCs to the regional lymph node. Expression of costimulatory markers and inflammatory cytokines was unaffected, consistent with homeostatic migration. In addition, levels of p-SMAD2/3 were decreased in LCs from wild-type mice before inflammation-induced migration. We conclude that TGF-β1 acts directly on LCs in an autocrine/paracrine manner to inhibit steady-state and inflammation-induced migration. This is a readily targetable pathway with potential therapeutic implications for skin disease.
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.