ReviewJournal of molecular medicine (Berlin, Germany)2011
Danger signals activating innate immunity in graft-versus-host disease.
Review in Journal of molecular medicine (Berlin, Germany), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 106 citations in OpenAlex.
- Upregulation of IFN-Inducible and Damage-Response Pathways in Chronic Graft-versus-Host Disease.Journal of immunology (Baltimore, Md. : 1950) · 2016Trial
- Identification and validation of biomarkers associated with acute and chronic graft versus host disease.Bone marrow transplantation · 2015Trial
- Utilization of Clinical Data and Evaluation of Biomarkers in the Investigation of Graft-Versus-Host Disease Outcomes.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Optimal GVHD Prophylaxis.Advances in experimental medicine and biology · 2025Review
- The effect of danger-associated molecular patterns on survival in acute graft versus host disease.Bone marrow transplantation · 2024Article
- Prevention of M2 polarization and temporal limitation of differentiation in monocytes by extracellular ATP.BMC immunology · 2023Article
- ER stress: an emerging regulator in GVHD development.Frontiers in immunology · 2023Review
- HTLV-1 infection of donor-derived T cells might promote acute graft-versus-host disease following liver transplantation.Nature communications · 2022Article
- Pre-Conditioning Serum Uric Acid as a Risk Factor for Sinusoidal Obstruction Syndrome of the Liver in Children Undergoing Hematopoietic Stem Cell TransplantationTurkish journal of haematology : official journal of Turkish Society of Haematology · 2021Article
- The NLRP3 Inflammasome: Relevance in Solid Organ Transplantation.International journal of molecular sciences · 2021Review
- Cascade of Inflammatory, Fibrotic Processes, and Stress-Induced Senescence in Chronic GVHD-Related Dry Eye Disease.International journal of molecular sciences · 2021Review
- Acute Graft-Frontiers in immunology · 2021Review
- Non-Coding RNAs: Master Regulators of Inflammasomes in Inflammatory Diseases.Journal of inflammation research · 2021Review
- The role of serum uric acid in the prediction of graft-versus-host disease in allogeneic hematopoietic stem cell transplantation.Journal of clinical laboratory analysis · 2020Article
- The Nlrp3 inflammasome as a "rising star" in studies of normal and malignant hematopoiesis.Leukemia · 2020Review
- Extracellular Adenosine Triphosphate (eATP) and Its Metabolite, Extracellular Adenosine (eAdo), as Opposing "Yin-Yang" Regulators of Nlrp3 Inflammasome in the Trafficking of Hematopoietic Stem/Progenitor Cells.Frontiers in immunology · 2020Review
- Article
- Host MyD88 signaling protects against acute graft-versus-host disease after allogeneic bone marrow transplantation.Clinical and experimental immunology · 2019Article
- Biology-driven developments in the therapy of acute graft-versus-host disease.Hematology. American Society of Hematology. Education Program · 2018Review
- [Cutaneous graft-versus-host disease].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extensive cell death with consecutive release of danger signals can cause immune-mediated tissue destruction. The abundance of cell death is likely to determine the relevance of the danger signals as physiological mechanisms that counteract immune activation may be overruled. Such constellation is conceivable in chemo-/radiotherapy-induced tissue damage, reperfusion injury, trauma, and severe infection. Studies on graft-versus-host disease (GvHD) development have to consider the effects of chemo-/radiotherapy-related tissue damage leading to the release of exogenous and endogenous danger signals. Our previous work has demonstrated a role for adenosine-5'-triphosphate (ATP) as an endogenous danger signal in GvHD. Besides ATP, uric acid or soluble extracellular matrix components are functional danger signals that activate the NLRP3 inflammasome when released from dying cells or from extracellular matrix. In contrast to sterile inflammation, GvHD is more complex since bacterial components that leak through damaged intestinal barriers and the skin can activate pattern recognition receptors and directly contribute to GvHD pathogenesis. These exogenous danger signals transmit immune activation via toll-like receptors and NOD-like receptors of the innate immune system. This review covers both the impact of endogenous and exogenous danger signals activating innate immunity in GvHD.
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.