Evidence map›Paper›PMID 37567982›Full record

ArticleScientific reports2023

Genetic manipulation resulting in decreased donor chondroitin sulfate synthesis mitigates hepatic GVHD via suppression of T cell activity.

Suguru Tamura, Hajime Ishiguro, Tatsuya Suwabe, Takayuki Katagiri, Kaori Cho, Kyoko Fuse, Yasuhiko Shibasaki, Tadahisa Mikami, Takero Shindo, Hiroshi Kitagawa and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 72% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

14 authors at 4 institutions in 1 country.

Suguru TamuraDepartment of Hematology, Niigata University Faculty of Medicine, 1-757 Asahimachi-dori, Chuo-ku, Niigata City, Niigata, 951-8510, Japan.
Hajime IshiguroDepartment of Hematology, Niigata University Faculty of Medicine, 1-757 Asahimachi-dori, Chuo-ku, Niigata City, Niigata, 951-8510, Japan.
Tatsuya SuwabeDepartment of Hematology, Niigata University Faculty of Medicine, 1-757 Asahimachi-dori, Chuo-ku, Niigata City, Niigata, 951-8510, Japan.
Takayuki KatagiriDepartment of Hematology, Niigata University Faculty of Medicine, 1-757 Asahimachi-dori, Chuo-ku, Niigata City, Niigata, 951-8510, Japan.
Kaori ChoDepartment of Hematology, Niigata University Faculty of Medicine, 1-757 Asahimachi-dori, Chuo-ku, Niigata City, Niigata, 951-8510, Japan.
Kyoko FuseDepartment of Hematology, Niigata University Faculty of Medicine, 1-757 Asahimachi-dori, Chuo-ku, Niigata City, Niigata, 951-8510, Japan.
Yasuhiko ShibasakiDepartment of Hematology, Niigata University Faculty of Medicine, 1-757 Asahimachi-dori, Chuo-ku, Niigata City, Niigata, 951-8510, Japan.
Tadahisa MikamiLaboratory of Biochemistry, Kobe Pharmaceutical University, Kobe, Japan.
Takero ShindoDepartment of Hematology/Oncology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hiroshi KitagawaLaboratory of Biochemistry, Kobe Pharmaceutical University, Kobe, Japan.
Michihiro IgarashiDepartment of Neurochemistry and Molecular Cell Biology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Hirohito SoneDepartment of Hematology, Niigata University Faculty of Medicine, 1-757 Asahimachi-dori, Chuo-ku, Niigata City, Niigata, 951-8510, Japan.
Masayoshi MasukoDepartment of Hematology, Niigata University Faculty of Medicine, 1-757 Asahimachi-dori, Chuo-ku, Niigata City, Niigata, 951-8510, Japan.
Takashi UshikiDepartment of Hematology, Niigata University Faculty of Medicine, 1-757 Asahimachi-dori, Chuo-ku, Niigata City, Niigata, 951-8510, Japan. tushiki@med.niigata-u.ac.jp.
Niigata University · JPNiigata University Medical and Dental Hospital · JPKobe Pharmaceutical University · JPKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Donor T cell activation, proliferation, differentiation, and migration are the major steps involved in graft-versus-host disease (GVHD) development following bone marrow transplantation. Chondroitin sulfate (CS) proteoglycan is a major component of the extracellular matrix and causes immune modulation by interacting with cell growth factors and inducing cell adhesion. However, its precise effects on immune function are unclear than those of other proteoglycan families. Thus, we investigated the significance of CS within donor cells in acute GVHD development utilizing CSGalNAc T1-knockout (T1KO) mice. To determine the effects of T1KO, the mice underwent allogenic bone marrow transplantation from major histocompatibility complex-mismatched donors. While transplantation resulted in hepatic GVHD with inflammatory cell infiltration of both CD4

Indexed as

Graft vs Host DiseaseHematopoietic Stem Cell TransplantationAnimalsBone Marrow TransplantationChondroitin SulfatesMiceMice, Inbred C57BLTransplantation, HomologousChondroitin Sulfates

Identifiers

PMID37567982
PMCPMC10421903
OpenAlexW4385760015

What OpenQuestion holds

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Registered trials

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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.