Evidence map›Paper›PMID 24683186›Full record

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

Cell depletion in mice that express diphtheria toxin receptor under the control of SiglecH encompasses more than plasmacytoid dendritic cells.

Melissa Swiecki, Yaming Wang, Elena Riboldi, Alfred H J Kim, Amiran Dzutsev, Susan Gilfillan, William Vermi, Christiane Ruedl, Giorgio Trinchieri, Marco Colonna

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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Thymic Dendritic Cells Revisited.Immunological reviews · 2025
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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

10 authors at 5 institutions in 3 countries.

Melissa SwieckiDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110;
Yaming Wang
Elena Riboldi
Alfred H J Kim
Amiran Dzutsev
Susan Gilfillan
William Vermi
Christiane Ruedl
Giorgio Trinchieri
Marco Colonna
Washington University in St. Louis · USNational Cancer Institute · USNanyang Technological University · SGUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITUniversity of Brescia · IT

Funding

Role of mouse microbiome in cancer and inflammationZIABC011153 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TRINCHIERI, GIORGIO · 2009 to 2025
$22.0M
Role of inflammation, innate resistance, and immunity in carcinogenesis.ZIABC010793 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TRINCHIERI, GIORGIO · 2009 to 2025
$16.8M
PRINCIPLES IN PULMONARY RESEARCHT32HL007317 · NHLBI · WASHINGTON UNIVERSITY · PI Steven Brody, Michael J Holtzman · 1985 to 2026
$16.1M
IMPACT OF PLASMACYTOID DENDRITIC CELLS ON TYPE I DIABETES PATHOGENESISK01DK095972 · NIDDK · WASHINGTON UNIVERSITY · PI SWIECKI, MELISSA · 2013 to 2014
$168k
NHLBI NIH HHS 2T32HL007317-31NHLBI NIH HHS T32 HL007317NIDDK NIH HHS 1K01DK095972-01A1NIDDK NIH HHS K01 DK095972
6 · The paper itself

Abstract

Plasmacytoid dendritic cells (pDC) produce IFN-I in response to viruses and are routinely identified in mice by SiglecH expression. SiglecH is a sialic acid-binding Ig-like lectin that has an immunomodulatory role during viral infections. In this study, we evaluated the impact of SiglecH deficiency on cytokine responses in the presence and absence of pDC. We found that lack of SiglecH enhanced IFN-I responses to viral infection, regardless of whether pDC were depleted. We also examined the expression pattern of SiglecH and observed that it was expressed by specialized macrophages and progenitors of classical dendritic cells and pDC. Accordingly, marginal zone macrophages and pDC precursors were eliminated in newly generated SiglecH-diphtheria toxin receptor (DTR)-transgenic (Tg) mice but not in CLEC4C-DTR-Tg mice after diphtheria toxin (DT) treatment. Using two bacterial models, we found that SiglecH-DTR-Tg mice injected with DT had altered bacterial uptake and were more susceptible to lethal Listeria monocytogenes infection than were DT-treated CLEC4C-DTR-Tg mice. Taken together, our findings suggest that lack of SiglecH may affect cytokine responses by cell types other than pDC during viral infections, perhaps by altering viral distribution or burden, and that cell depletion in SiglecH-DTR-Tg mice encompasses more than pDC.

Indexed as

AnimalsCell SeparationCytokinesDendritic CellsDiphtheria ToxinEnzyme-Linked Immunosorbent AssayFlow CytometryFluorescent Antibody TechniqueGene Knock-In TechniquesHeparin-binding EGF-like Growth FactorImmunohistochemistryInfectionsIntercellular Signaling Peptides and ProteinsLectinsMacrophagesMiceCytokinesDiphtheria ToxinHbegf protein, mouseHeparin-binding EGF-like Growth FactorIntercellular Signaling Peptides and ProteinsLectinsReceptors, Cell SurfaceSiglech protein, mouse

Identifiers

PMID24683186
PMCPMC4194082
OpenAlexW2118403843

What OpenQuestion holds

Textmetadata
LicenceTDM
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.