ArticlePloS one2016
IL-15 Superagonist Expands mCD8+ T, NK and NKT Cells after Burn Injury but Fails to Improve Outcome during Burn Wound Infection.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 30 citations in OpenAlex.
- Exploring the impact of IL-2 cytokine family on skin barrier function: pathophysiology and therapeutic strategies.Molecular biology reports · 2026Review
- GM-CSF ameliorates inflammation from Pseudomonas aeruginosa in a juvenile mouse model of burn injury.Journal of leukocyte biology · 2025Article
- Immunoresponsive gene 1 facilitates TLR4 agonist-induced augmentation of innate antimicrobial immunity.Journal of leukocyte biology · 2025Article
- Lymphopenia in sepsis: a narrative review.Critical care (London, England) · 2024Review
- Prediction of immune molecules activity during burn wound healing among elderly patients: in-silico analyses: experimental research.Annals of medicine and surgery (2012) · 2024Article
- Natural killer cells in sepsis: Friends or foes?Frontiers in immunology · 2023Review
- Review
- A novel membrane-bound interleukin-2 promotes NK-92 cell persistence and anti-tumor activity.Oncoimmunology · 2022Article
- Identification of Important Modules and Biomarkers That Are Related to Immune Infiltration Cells in Severe Burns Based on Weighted Gene Co-Expression Network Analysis.Frontiers in genetics · 2022Article
- Interleukin-15 and cancer: some solved and many unsolved questions.Journal for immunotherapy of cancer · 2020Review
- Article
- Review
- CD4 T Cell Responses and the Sepsis-Induced Immunoparalysis State.Frontiers in immunology · 2020Review
- Polymicrobial sepsis influences NK-cell-mediated immunity by diminishing NK-cell-intrinsic receptor-mediated effector responses to viral ligands or infections.PLoS pathogens · 2018Article
- Sepsis-Induced T Cell Immunoparalysis: The Ins and Outs of Impaired T Cell Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2018Review
- The biology of natural killer cells during sepsis.Immunology · 2018Review
- Frontline Science: Anti-PD-L1 protects against infection with common bacterial pathogens after burn injury.Journal of leukocyte biology · 2018Article
- Immunobiology of the IL-15/IL-15Rα complex as an antitumor and antiviral agent.Cytokine & growth factor reviews · 2017Review
- IL-15 Enables Septic Shock by Maintaining NK Cell Integrity and Function.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Flt3 Ligand Treatment Attenuates T Cell Dysfunction and Improves Survival in a Murine Model of Burn Wound Sepsis.Shock (Augusta, Ga.) · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSeverely burned patients are highly susceptible to opportunistic infections and sepsis, owing to the loss of the protective skin barrier and immunological dysfunction. Interleukin-15 (IL-15) belongs to the IL-2 family of common gamma chain cytokines and stimulates the proliferation and activation of T (specifically memory CD8), NK and NKT cells. It has been shown to preserve T cell function and improve survival during cecal ligation and puncture (CLP)-induced sepsis in mice. However, the therapeutic efficacy of IL-15 or IL-15 superagonist (SA) during infection after burn injury has not been evaluated. Moreover, very few, if any, studies have examined, in detail, the effect of burn injury and infection on the adaptive immune system. Thus, we examined the effect of burn and sepsis on adaptive immune cell populations and the effect of IL-15 SA treatment on the host response to infection.
methodsMice were subjected to a 35% total body surface area burn, followed by wound infection with Pseudomonas aeruginosa. In some experiments, IL-15 SA was administered after burn injury, but before infection. Leukocytes in spleen, liver and peritoneal cavity were characterized using flow cytometry. Bacterial clearance, organ injury and survival were also assessed.
resultsBurn wound infection led to a significant decline in total white blood cell and lymphocyte counts and induced organ injury and sepsis. Burn injury caused decline in CD4+ and CD8+ T cells in the spleen, which was worsened by infection. IL-15 treatment inhibited this decline and significantly increased cell numbers and activation, as determined by CD69 expression, of CD4+, CD8+, B, NK and NKT cells in the spleen and liver after burn injury. However, IL-15 SA treatment failed to prevent burn wound sepsis-induced loss of CD4+, CD8+, B, NK and NKT cells and failed to improve bacterial clearance and survival.
conclusionCutaneous burn injury and infection cause significant adaptive immune dysfunction. IL-15 SA does not augment host resistance to burn wound sepsis in mice despite inducing proliferation and activation of lymphocyte subsets.
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.