ArticleThe Journal of trauma2011
Th17 (IFNγ- IL17+) CD4+ T cells generated after burn injury may be a novel cellular mechanism for postburn immunosuppression.
Article in The Journal of trauma, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Determination of Burn Size in Mouse Models of Burn Injury: A Scoping Review of Studies Leveraging Scald and Contact Burns.Journal of burn care & research : official publication of the American Burn Association · 2025Pooled it
- Focal Adhesion Kinase Inhibition Ameliorates Burn Injury-Induced Chronic Pain in Rats.Molecular neurobiology · 2025Article
- Sepsis prevents the development of experimental type 1 diabetes.Frontiers in immunology · 2025Article
- Unremitting pro-inflammatory T-cell phenotypes, and macrophage activity, following paediatric burn injury.Clinical & translational immunology · 2024Article
- Multidrug-Resistant Gram-Negative Bacteria in Burn Patients.Antimicrobial agents and chemotherapy · 2022Article
- Molecular imbalance mechanism of skin and blood leucocytes in severe burn patients at different burn times.Annals of translational medicine · 2022Article
- OX40-Fc Fusion Protein Alleviates PD-1-Fc-Aggravated Rheumatoid Arthritis by Inhibiting Inflammatory Response.Computational and mathematical methods in medicine · 2022Article
- Mechanism of pulmonary immunosuppression: extrapulmonary burn injury suppresses bacterial endotoxin-induced pulmonary neutrophil recruitment and neutrophil extracellular trap (NET) formation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Article
- Neutralization of interleukin-17A alleviates burn-induced intestinal barrier disruption via reducing pro-inflammatory cytokines in a mouse model.Burns & trauma · 2019Article
- HMGB1/IL-1β complexes in plasma microvesicles modulate immune responses to burn injury.PloS one · 2018Article
- Risk Factors for Healthcare-Associated Infections in Adult Burn Patients.Infection control and hospital epidemiology · 2017Article
- 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
- Innate Immune Cell Recovery Is Positively Regulated by NLRP12 during Emergency Hematopoiesis.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Timeline of health care-associated infections and pathogens after burn injuries.American journal of infection control · 2016Article
- Association between early airway damage-associated molecular patterns and subsequent bacterial infection in patients with inhalational and burn injury.American journal of physiology. Lung cellular and molecular physiology · 2015Observational
- Dynamic changes of circulating T-helper cell subsets following severe thoracic trauma.International journal of clinical and experimental medicine · 2015Article
- Reduction in central line-associated bloodstream infections in patients with burns.Infection control and hospital epidemiology · 2014Article
- The role of aryl hydrocarbon receptor in interleukin-23-dependent restoration of interleukin-22 following ethanol exposure and burn injury.Annals of surgery · 2014Article
- Functional modularity of the arginine catabolic mobile element contributes to the success of USA300 methicillin-resistant Staphylococcus aureus.Cell host & microbe · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe mechanism responsible for initiating and controlling the immunosuppressive response after burn injury remains unknown. Interleukin-17 (IL-17) secreting Th17 (interferon [IFN]γ IL17) cells are a novel subset of CD4 T cells associated with a weak, proinflammatory response that antagonizes the proinflammatory Th1 (IFNγ IL17) response. Given that transforming growth factor-β and IL6 mediate Th17 cell development, we hypothesized that burn injury may generate Th17 cells that could mediate postburn immunosuppression.
methodsAfter a 20% total body surface area burn in female C57BL/6 mice, wound-draining lymph nodes were harvested 3 days, 7 days, or 14 days after injury. CD4 T cells were enriched by magnetic selection, and flow cytometry was used to identify intracellular IL17 and IFNγ in CD3CD4 T cells. Additional purified CD3CD4 T cells were cultured with Th17 polarizing IL6 and transforming growth factor-β for 4 days, and flow cytometry was again used to identify intracellular IL17 and IFNγ in CD4 T cells.
resultsThe number and percentage of preformed Th17 cells was significantly greater in burn mice compared with sham at all time points. In addition, the ratio of Th17 cells to Th1 cells was always significantly higher in burn mice compared with sham. These differences were eliminated in Th17 polarizing conditions in vitro. CD4 T cells never generated both IL17 and IFNγ.
conclusionThese results demonstrate for the first time that Th17 cells (IFNγ IL17) are spontaneously generated after burn injury. Given that Th17 cells (IFNγ IL17) are antagonistic to Th1 (IFNγ IL17) cells, these results suggest a novel mechanism for initiating and controlling postburn immunosuppression that deserves further investigation.
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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.