ArticleBlood2016
TNF-α priming enhances CD4+FoxP3+ regulatory T-cell suppressive function in murine GVHD prevention and treatment.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
What it found
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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
73 citing papers in PubMed, 113 citations in OpenAlex.
- Mapping the TNFR2-targeting antibody patent landscape: Insights from macro trends to structural signatures.Human vaccines & immunotherapeutics · 2026Article
- Decoding TNF receptor superfamily control of CD4Cell communication and signaling : CCS · 2026Review
- Review
- Cytokines Associated with Activation of CD4International journal of molecular sciences · 2026Review
- TRIP13 promotes the expansion and immunosuppression of CD4Cell death & disease · 2026Article
- Development of a humanized mouse model of graft-versus-host disease to assess human regulatory T cell function.Frontiers in immunology · 2025Article
- Current status, challenges, and integration pathways of biomarker classification systems in graft-versus-host disease: a preliminary exploration.Frontiers in medicine · 2025Review
- Recent advances and research progress regarding monoclonal antibodies for chronic graft-versus-host disease.Heliyon · 2024Review
- How adoptive transfer of components of the donor immune system boosts GvL and prevents GvHD in HLA-haploidentical hematopoietic transplantation for acute leukemia.Bone marrow transplantation · 2024Review
- Suppression of P53 Pathway is an Important Factor Inducing Acute Graft-versus-Host Disease Through T Cell Activation Based on Bioinformatics Analysis.Journal of inflammation research · 2024Article
- Longitudinal dynamics of gut microbiota in the pathogenesis of acute graft-versus-host disease.Cancer medicine · 2023Article
- Assessment of the Potential Role of Selected Single Nucleotide Polymorphisms (SNPs) of Genes Related to the Functioning of Regulatory T Cells in the Pathogenesis of Psoriasis.International journal of molecular sciences · 2023Article
- Article
- The role of TNF-α in the fate regulation and functional reprogramming of mesenchymal stem cells in an inflammatory microenvironment.Frontiers in immunology · 2023Review
- TNFR2 antagonist and agonist: a potential therapeutics in cancer immunotherapy.Medical oncology (Northwood, London, England) · 2022Review
- TNF blockade enhances the efficacy of myxoma virus-based oncolytic virotherapy.Journal for immunotherapy of cancer · 2022Article
- Mesenchymal stem cells transfer mitochondria to allogeneic Tregs in an HLA-dependent manner improving their immunosuppressive activity.Nature communications · 2022Article
- Article
- TFNR2 in Ischemia-Reperfusion Injury, Rejection, and Tolerance in Transplantation.Frontiers in immunology · 2022Review
- A Promising Insight: The Potential Influence and Therapeutic Value of the Gut Microbiota in GI GVHD.Oxidative medicine and cellular longevity · 2022Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
CD4(+)CD25(+)FoxP3(+) regulatory T cells (Tregs) have been shown to effectively prevent graft-versus-host disease (GVHD) when adoptively transferred in murine models of hematopoietic cell transplantation and in phase 1/2 clinical trials. Critical limitations to Treg clinical application are the paucity of cells and limited knowledge of the mechanisms of in vivo function. We hypothesized that inflammatory conditions in GVHD modify Treg characteristics and activity. We found that peripheral blood of recipient animals during acute GVHD (aGVHD) induces Treg activation and enhances their function. The serum contains high levels of tumor necrosis factor-α (TNF-α) that selectively activates Tregs without impacting CD4(+)FoxP3(-) T cells. TNF-α priming induces Treg in vivo proliferation, whereas it limits the ability of CD4 and CD8 conventional T cells (Tcons) to proliferate and induce GVHD. TNF-α-primed Tregs prolong animal survival as compared with unprimed Tregs when used at an unfavorable Treg:Tcon ratio, demonstrating enhanced in vivo efficacy of TNF-α-primed Tregs. Because TNF-α is produced by several immune cells during inflammation, our work elucidates aspects of the physiologic mechanisms of Treg function. Furthermore, TNF-α priming of Tregs provides a new tool to optimize Treg cellular therapies for GVHD prevention and treatment.
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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.