ArticleEuropean journal of immunology2010
Impaired CD4+ T-cell proliferation and effector function correlates with repressive histone methylation events in a mouse model of severe sepsis.
Article in European journal of immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Epigenetic mechanisms of Immune remodeling in sepsis: targeting histone modification.Cell death & disease · 2023Pooled it
- Immunology of Sepsis.Clinics in chest medicine · 2026Review
- MYSM1-mediated epigenetic modification dysregulation leads to immunosuppression and secondary infections in sepsis.PLoS pathogens · 2026Article
- The Epigenetics of Sepsis: How Gene Modulation Shapes Outcomes.Biomedicines · 2025Review
- Lymphopenia in sepsis: a narrative review.Critical care (London, England) · 2024Review
- Metabolic reprogramming and dysregulated IL-17 production impairs CD4 T cell function post sepsis.iScience · 2024Article
- Regulatory T lymphocytes in traumatic brain injury.Neurochemistry international · 2024Review
- Advances in Immune Monitoring Approaches for Sepsis-Induced Immunosuppression.Frontiers in immunology · 2022Review
- Sepsis and multiple sclerosis: Causative links and outcomes.Immunology letters · 2021Review
- Immune Cell Number, Phenotype, and Function in the Elderly with Sepsis.Aging and disease · 2021Review
- Exploring the pathophysiology of post-sepsis syndrome to identify therapeutic opportunities.EBioMedicine · 2020Review
- Screening key genes and microRNAs in sepsis by RNA-sequencing.Journal of the Chinese Medical Association : JCMA · 2020Article
- CD4 T Cell Responses and the Sepsis-Induced Immunoparalysis State.Frontiers in immunology · 2020Review
- Lipopolysaccharide suppresses T cells by generating extracellular ATP that impairs their mitochondrial function via P2Y11 receptors.The Journal of biological chemistry · 2019Article
- Abrogated Caveolin-1 expression via histone modification enzyme Setdb2 regulates brain edema in a mouse model of influenza-associated encephalopathy.Scientific reports · 2019Article
- Advances in the understanding and treatment of sepsis-induced immunosuppression.Nature reviews. Nephrology · 2018Review
- The protective role of human ghrelin in sepsis: Restoration of CD4 T cell proliferation.PloS one · 2018Article
- Desperate Times Call for Desperate Measures: Self-Cannibalism Is Protective During Sepsis.Critical care medicine · 2017Article
- Role of cellular events in the pathophysiology of sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016Review
- Role of epigenetics in modulation of immune response at the junction of host-pathogen interaction and danger molecule signaling.Pathogens and disease · 2016Article
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
Immunosuppression following severe sepsis remains a significant human health concern, as long-term morbidity and mortality rates of patients who have recovered from life-threatening septic shock remain poor. Mouse models of severe sepsis indicate this immunosuppression may be partly due to alterations in myeloid cell function; however, the effect of severe sepsis on subsequent CD4(+) T-cell responses remains unclear. In the present study, CD4(+) T cells from mice subjected to an experimental model of severe sepsis (cecal ligation and puncture (CLP)) were analyzed in vitro. CD4(+)CD62L(+) T cells from CLP mice exhibited reduced proliferative capacity and altered gene expression. Additionally, CD4(+)CD62L(+) T cells from CLP mice exhibit dysregulated cytokine production after in vitro skewing with exogenous cytokines, indicating a decreased capability of these cells to commit to either the T(H)1 or T(H)2 lineage. Repressive histone methylation marks were also evident at promoter regions for the T(H)1 cytokine IFN-gamma and the T(H)2 transcription factor GATA-3 in naïve CD4(+) T cells from CLP mice. These results provide evidence that CD4(+) T-cell subsets from post-septic mice exhibit defects in activation and effector function, possibly due to chromatin remodeling proximal to genes involved in cytokine production or gene transcription.
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.