ArticleCytokine2012
Gamma delta (γδ) T-cells are critical in the up-regulation of inducible nitric oxide synthase at the burn wound site.
Article in Cytokine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Histological efficacy of high-dose intravenous vitamin C infusion in severely burned patients.Journal of molecular histology · 2025Article
- Roles of dendritic epidermal T cells in steady and different pathological states.Burns & trauma · 2025Review
- Spatiotemporal orchestration of macrophage activation trajectories by Vγ4 T cells during skin wound healing.iScience · 2024Article
- Li-Hong Tang alleviates dextran sodium sulfate-induced colitis by regulating NRF2/HO-1 signaling pathway and gut microbiota.Frontiers in pharmacology · 2024Article
- The molecular mechanisms supporting the homeostasis and activation of dendritic epidermal T cell and its role in promoting wound healing.Burns & trauma · 2021Review
- Immunological approaches and therapy in burns (Review).Experimental and therapeutic medicine · 2020Review
- Article
- The Role of Th-17 Cells and γδ T-Cells in Modulating the Systemic Inflammatory Response to Severe Burn Injury.International journal of molecular sciences · 2017Review
- Article
- Heterogeneity of mast cells and expression of Annexin A1 protein in a second degree burn model with silver sulfadiazine treatment.PloS one · 2017Article
- Dermal γδ T-Cells Can Be Activated by Mitochondrial Damage-Associated Molecular Patterns.PloS one · 2016Article
- Chronic Inflammation and γδ T Cells.Frontiers in immunology · 2016Review
- Fat Grafting in Burn Scar Alleviates Neuropathic Pain via Anti-Inflammation Effect in Scar and Spinal Cord.PloS one · 2015Article
- Gamma delta T cells regulate wound myeloid cell activity after burn.Shock (Augusta, Ga.) · 2014Article
- Adipose inflammation and macrophage infiltration after binge ethanol and burn injury.Alcoholism, clinical and experimental research · 2014Article
- γδ T Cell-Mediated Immune Responses in Disease and Therapy.Frontiers in immunology · 2014Review
- Burn wound γδ T-cells support a Th2 and Th17 immune response.Journal of burn care & research : official publication of the American Burn AssociationArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe high incidence of morbidity and mortality following major burn can in part be attributed to immune derangements and wound healing complications. Inflammation plays an important role in wound healing, of which inducible nitric oxide synthase (iNOS) derived nitric oxide is a central mediator. T-cells of the γδ TCR lineage have also been shown to be important in healing of the burn wound site. Nonetheless, the role of γδ T-cells in the regulation of the burn wound iNOS expression is unknown.
methodsWildtype (WT) and δ TCR(-/-) male C57BL/6 mice were subjected to burn (3rd degree, 12.5% TBSA) or sham treatment. Three days after injury, skin samples from non-injured and the burn wound were collected and analyzed for the expression of iNOS and cytokines and chemokine levels. In a second series of experiments, WT mice were subjected to burn and left untreated or treated with the iNOS inhibitor, L-Nil. Skin cytokine and chemokine levels were assessed 3days thereafter.
resultsBurn induced an 18-fold increase in iNOS expression at the wound site as compared to the uninjured skin of WT sham mice. In δ TCR(-/-) mice iNOS expression at the wound site was significantly lower than that of the WT group. Burn also induced increased levels of IL-1β, IL-6, G-CSF, TNF-α, KC, MCP-1, MIP-1α and MIP-1β at the wound site in WT and δ TCR(-/-) mice, but G-CSF, TNF-α, and MIP-1β levels were greater in δ TCR(-/-) mice. Inhibition of iNOS activity in WT mice with L-Nil suppressed burn wound levels of IL-1β, G-CSF, and MIP-1α, whereas IL-6, TNF-α, KC, MCP-1 and MIP-1β were unaffected.
conclusionsT-cells of the γδ TCR lineage significantly contribute to the up-regulation of iNOS expression which contributes to wound inflammation.
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