ArticleThe Journal of clinical investigation2014
Hyaluronan digestion controls DC migration from the skin.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 80 citations in OpenAlex.
- Angiogenesis, Angiogenic Factors, and Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS).International journal of urology : official journal of the Japanese Urological Association · 2026Review
- Sulfated Glycosaminoglycans in Inflammation.Advances in experimental medicine and biology · 2026Review
- The gut-skin axis: a bi-directional, microbiota-driven relationship with therapeutic potential.Gut microbes · 2025Review
- CD44 signaling in skin wound healing and regeneration.Journal of translational medicine · 2025Review
- Low-molecular-weight hyaluronic acid improves regeneration of cystic fibrosis airway epithelium.ERJ open research · 2025Article
- Innate and Adaptive Immune Responses to Clinical Hyaluronic Acid Fillers.Journal of cosmetic dermatology · 2025Article
- Targeting inflammatory macrophages with hyaluronan tetrasaccharide: effects on fibroblast collagen degradation and synthesis.Frontiers in immunology · 2025Article
- Dermal injury drives a skin to gut axis that disrupts the intestinal microbiome and intestinal immune homeostasis in mice.Nature communications · 2024Article
- Contributions of PD-L1 reverse signaling to dendritic cell trafficking.The FEBS journal · 2022Review
- Modulation of hyaluronan signaling as a therapeutic target in human disease.Pharmacology & therapeutics · 2022Review
- Skin inflammation activates intestinal stromal fibroblasts and promotes colitis.The Journal of clinical investigation · 2021Article
- Formulation-based approaches for dermal delivery of vaccines and therapeutic nucleic acids: Recent advances and future perspectives.Bioengineering & translational medicine · 2021Review
- Contact dermatitis.Nature reviews. Disease primers · 2021Review
- Hyaluronan is a natural and effective immunological adjuvant for protein-based vaccines.Cellular & molecular immunology · 2021Article
- PD-L1 Reverse Signaling in Dermal Dendritic Cells Promotes Dendritic Cell Migration Required for Skin Immunity.Cell reports · 2020Article
- NLRP3 Inflammasome and Allergic Contact Dermatitis: A Connection to Demystify.Pharmaceutics · 2020Review
- [Extended understanding of pathogenesis and treatment of contact allergy].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2020Review
- Hyaluronan Degradation by Cemip Regulates Host Defense against Staphylococcus aureus Skin Infection.Cell reports · 2020Article
- Hyaluronidase-4 is produced by mast cells and can cleave serglycin chondroitin sulfate chains into lower molecular weight forms.The Journal of biological chemistry · 2019Article
- Hyaluronan in immune dysregulation and autoimmune diseases.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The breakdown and release of hyaluronan (HA) from the extracellular matrix has been hypothesized to act as an endogenous signal of injury. To test this hypothesis, we generated mice that conditionally overexpressed human hyaluronidase 1 (HYAL1). Mice expressing HYAL1 in skin either during early development or by inducible transient expression exhibited extensive HA degradation, yet displayed no evidence of spontaneous inflammation. Further, HYAL1 expression activated migration and promoted loss of DCs from the skin. We subsequently determined that induction of HYAL1 expression prior to topical antigen application resulted in a lack of an antigenic response due to the depletion of DCs from the skin. In contrast, induction of HYAL1 expression concurrent with antigen exposure accelerated allergic sensitization. Administration of HA tetrasaccharides, before or simultaneously with antigen application, recapitulated phenotypes observed in HYAL1-expressing animals, suggesting that the generation of small HA fragments, rather than the loss of large HA molecules, promotes DC migration and subsequent modification of allergic responses. Furthermore, mice lacking TLR4 did not exhibit HA-associated phenotypes, indicating that TLR4 mediates these responses. This study provides direct evidence that HA breakdown controls the capacity of the skin to present antigen. These events may influence DC function in injury or disease and have potential to be exploited therapeutically for modification of allergic responses.
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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.