Evidence map›Paper›PMID 23113638›Full record

ArticleImmunology2013

The DC-HIL ligand syndecan-4 is a negative regulator of T-cell allo-reactivity responsible for graft-versus-host disease.

Jin-Sung Chung, Mizuki Tomihari, Kyoichi Tamura, Tetsuhito Kojima, Ponciano D Cruz, Kiyoshi Ariizumi

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Glycoprotein nonmetastatic melanoma protein B: A key mediator and an emerging therapeutic target in autoimmune diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Syndecan-4 signaling at a glance.Journal of cell science · 2013
    Review
  13. Article
  14. Article
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

6 authors at 3 institutions in 2 countries.

Jin-Sung ChungDepartment of Dermatology, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Mizuki Tomihari
Kyoichi Tamura
Tetsuhito Kojima
Ponciano D Cruz
Kiyoshi Ariizumi
The University of Texas Southwestern Medical Center · USNagoya University · JPVeterans Health Administration · US

Funding

DC-HIL in Cutaneous ImmunityR01AI064927 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI ARIIZUMI, KIYOSHI · 2005 to 2014
$3.1M
DC-HIL in Cutaneous ImmunityR56AI064927 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI ARIIZUMI, KIYOSHI · 2009 to 2009
$393k
NIAID NIH HHS AI064927-05NIAID NIH HHS R01 AI064927NIAID NIH HHS R56 AI064927
6 · The paper itself

Abstract

Acute graft-versus-host disease (GVHD) is the most important cause of mortality after allogeneic haematopoietic stem cell transplantation. Allo-reactive T cells are the major mediators of GVHD and the process is regulated by positive and negative regulators on antigen-presenting cells (APC). Because the significance of negative regulators in GVHD pathogenesis is not fully understood, and having discovered that syndecan-4 (SD-4) on effector T cells mediates the inhibitory function of DC-HIL on APC, we proposed that SD-4 negatively regulates the T-cell response to allo-stimulation in acute GVHD, using SD-4 knockout mice. Although not different from their wild-type counterparts in responsiveness to anti-CD3 stimulation, SD-4(-/-) T cells lost the capacity to mediate the inhibitory function of DC-HIL and were hyper-reactive to allogeneic APC. Moreover, infusion of SD-4(-/-) T cells into sub-lethally γ-irradiated allogeneic mice worsened mortality, with hyper-proliferation of infused T cells in recipients. Although there my be little or no involvement of regulatory T cells in this model because SD-4 deletion had no deleterious effect on T-cell-suppressive activity compared with SD-4(+/+) regulatory T cells. We conclude that SD-4, as the T-cell ligand of DC-HIL, is a potent inhibitor of allo-reactive T cells responsible for GVHD and a potentially useful target for treating this disease.

Indexed as

Hematopoietic Stem Cell TransplantationAcute DiseaseAnimalsEye ProteinsGraft vs Host DiseaseMembrane GlycoproteinsMiceMice, Inbred BALB CMice, KnockoutReceptors, ImmunologicSyndecan-4T-Lymphocytes, RegulatoryTransplantation, HomologousEye ProteinsGpnmb protein, mouseMembrane GlycoproteinsReceptors, ImmunologicSdc4 protein, mouseSyndecan-4

Identifiers

PMID23113638
PMCPMC3575770
OpenAlexW1992767628

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.