Evidence map›Paper›PMID 24516197›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

The DC-HIL/syndecan-4 pathway regulates autoimmune responses through myeloid-derived suppressor cells.

Jin-Sung Chung, Kyoichi Tamura, Hideo Akiyoshi, Ponciano D Cruz, Kiyoshi Ariizumi

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
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  6. Article
  7. Review
  8. Article
  9. High-throughput single-сell sequencing in cancer research.Signal transduction and targeted therapy · 2022
    Review
  10. Article
  11. Article
  12. 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
  13. Blocking Monocytic Myeloid-Derived Suppressor Cell Function via Anti-DC-HIL/GPNMB Antibody Restores theClinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  14. Review
  15. The ratio of HLA-DR and VNN2Journal of neuro-oncology · 2017
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 3 institutions in 1 country.

Jin-Sung ChungDepartment of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX 75390.
Kyoichi Tamura
Hideo Akiyoshi
Ponciano D Cruz
Kiyoshi Ariizumi
Veterans Health Administration · USDallas VA Medical Center · USThe University of Texas Southwestern Medical Center · 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

Having discovered that the dendritic cell (DC)-associated heparan sulfate proteoglycan-dependent integrin ligand (DC-HIL) receptor on APCs inhibits T cell activation by binding to syndecan-4 (SD-4) on T cells, we hypothesized that the DC-HIL/SD-4 pathway may regulate autoimmune responses. Using experimental autoimmune encephalomyelitis (EAE) as a disease model, we noted an increase in SD-4(+) T cells in lymphoid organs of wild-type (WT) mice immunized for EAE. The autoimmune disease was also more severely induced (clinically, histologically, and immunophenotypically) in mice knocked out for SD-4 compared with WT cohorts. Moreover, infusion of SD-4(-/-) naive T cells during EAE induction into Rag2(-/-) mice also led to increased severity of EAE in these animals. Similar to SD-4 on T cells, DC-HIL expression was upregulated on myeloid cells during EAE induction, with CD11b(+)Gr-1(+) myeloid-derived suppressor cells (MDSCs) as the most expanded population and most potent T cell suppressor among the myeloid cells examined. The critical role of DC-HIL was supported by DC-HIL gene deletion or anti-DC-HIL treatment, which abrogated T cell suppressor activity of MDSCs, and also by DC-HIL activation inducing MDSC expression of IFN-γ, NO, and reactive oxygen species. Akin to SD-4(-/-) mice, DC-HIL(-/-) mice manifested exacerbated EAE. Adoptive transfer of MDSCs from EAE-affected WT mice into DC-HIL(-/-) mice reduced EAE severity to the level of EAE-immunized WT mice, an outcome that was precluded by depleting DC-HIL(+) cells from the infused MDSC preparation. Our findings indicate that the DC-HIL/SD-4 pathway regulates autoimmune responses by mediating the T cell suppressor function of MDSCs.

Indexed as

Adoptive TransferAnimalsAutoimmunityCD11b AntigenCells, CulturedDNA-Binding ProteinsEncephalomyelitis, Autoimmune, ExperimentalEye ProteinsFemaleFlow CytometryInterferon-gammaMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutMyeloid CellsCD11b AntigenDNA-Binding ProteinsEye ProteinsGpnmb protein, mouseGr-1 protein, mouseInterferon-gammaMembrane GlycoproteinsNitric OxideRag2 protein, mouseReactive Oxygen SpeciesReceptors, ChemokineSyndecan-4

Identifiers

PMID24516197
PMCPMC3957202
OpenAlexW2119116867

What OpenQuestion holds

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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.