Evidence map›Paper›PMID 25911749›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

The Free Radical Scavenger NecroX-7 Attenuates Acute Graft-versus-Host Disease via Reciprocal Regulation of Th1/Regulatory T Cells and Inhibition of HMGB1 Release.

Keon-Il Im, Nayoun Kim, Jung-Yeon Lim, Young-Sun Nam, Eun-Sol Lee, Eun-Jung Kim, Hyoung Jin Kim, Soon Ha Kim, Seok-Goo Cho

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.3field-weighted citation impact, top 5% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 52 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 3 countries.

Keon-Il ImInstitute for Translational Research and Molecular Imaging, Catholic Research Institute of Medical Science, Catholic University of Korea, Seoul 137-701, Korea; Laboratory of Immune Regulation, Convergent Research Consortium for Immunologic Disease, Catholic University of Korea College of Medicine, St. Mary's Hospital, Seoul 137-701, Korea;
Nayoun KimInstitute for Translational Research and Molecular Imaging, Catholic Research Institute of Medical Science, Catholic University of Korea, Seoul 137-701, Korea; Laboratory of Immune Regulation, Convergent Research Consortium for Immunologic Disease, Catholic University of Korea College of Medicine, St. Mary's Hospital, Seoul 137-701, Korea;
Jung-Yeon LimInstitute for Translational Research and Molecular Imaging, Catholic Research Institute of Medical Science, Catholic University of Korea, Seoul 137-701, Korea; Laboratory of Immune Regulation, Convergent Research Consortium for Immunologic Disease, Catholic University of Korea College of Medicine, St. Mary's Hospital, Seoul 137-701, Korea;
Young-Sun NamInstitute for Translational Research and Molecular Imaging, Catholic Research Institute of Medical Science, Catholic University of Korea, Seoul 137-701, Korea; Laboratory of Immune Regulation, Convergent Research Consortium for Immunologic Disease, Catholic University of Korea College of Medicine, St. Mary's Hospital, Seoul 137-701, Korea;
Eun-Sol LeeInstitute for Translational Research and Molecular Imaging, Catholic Research Institute of Medical Science, Catholic University of Korea, Seoul 137-701, Korea; Laboratory of Immune Regulation, Convergent Research Consortium for Immunologic Disease, Catholic University of Korea College of Medicine, St. Mary's Hospital, Seoul 137-701, Korea;
Eun-Jung KimLaboratory of Immune Regulation, Convergent Research Consortium for Immunologic Disease, Catholic University of Korea College of Medicine, St. Mary's Hospital, Seoul 137-701, Korea;
Hyoung Jin KimStrategy and Development, LG Life Sciences Ltd., Seoul 2305-738, Korea; and.
Soon Ha KimStrategy and Development, LG Life Sciences Ltd., Seoul 2305-738, Korea; and.
Seok-Goo ChoInstitute for Translational Research and Molecular Imaging, Catholic Research Institute of Medical Science, Catholic University of Korea, Seoul 137-701, Korea; Laboratory of Immune Regulation, Convergent Research Consortium for Immunologic Disease, Catholic University of Korea College of Medicine, St. Mary's Hospital, Seoul 137-701, Korea; Department of Hematology, Catholic Blood and Marrow Transplantation Center, Seoul St. Mary's Hospital, Catholic University of Korea College of Medicine, Seoul 137-701, Korea chosg@catholic.ac.kr.
Seoul St. Mary's Hospital · KRGlobal Strategy Group · USSt. Mary's Hospital · USCatholic University of Korea · KRSt Mary's Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Graft-versus-host disease (GVHD) is a major complication associated with allogeneic hematopoietic stem cell transplantation. Despite the prominent role of the adaptive immune system, the importance of controlling the innate immune system in the pathogenesis of GVHD has recently been rediscovered. High-mobility group box 1 (HMGB1) is a crucial damage-associated molecular pattern signal that functions as a potent innate immune mediator in GVHD. In the present study, we investigated treatment of experimental GVHD through HMGB1 blockade using the compound cyclopentylamino carboxymethylthiazolylindole (NecroX)-7. Treated animals significantly attenuated GVHD-related mortality and inhibited severe tissue damage. These protective effects correlated with the decrease in HMGB1 expression and lower levels of reactive oxidative stress. Additionally, NecroX-7 inhibited the HMGB1-induced release of TNF and IL-6, as well as the expression of TLR-4 and receptor for advanced glycation end products. We also observed increased regulatory T cell numbers, which may be associated with regulation of differentiation signals independent of HMGB1. Taken together, these data indicate that NecroX-7 protects mice against lethal GVHD by reciprocal regulation of regulatory T/Th1 cells, attenuating systemic HMGB1 accumulation and inhibiting HMGB1-mediated inflammatory response. Our results indicate the possibility of a new use for a clinical drug that is effective for the treatment of GVHD.

Indexed as

AnimalsCell DifferentiationCell LineCell ProliferationFemaleFree Radical ScavengersGraft vs Host DiseaseHematopoietic Stem Cell TransplantationHMGB1 ProteinInterleukin-6MiceMice, Inbred BALB CMice, Inbred C57BLMitochondriaOrganic ChemicalsOxidative StressFree Radical ScavengersHMGB1 ProteinHMGB1 protein, mouseInterleukin-6necrox-7Organic ChemicalsProtein Kinase CReactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsReceptors, ImmunologicTlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID25911749
PMCPMC4432727
OpenAlexW1619424850

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.