Evidence map›Paper›PMID 28642279›Full record

ArticleJournal of leukocyte biology2017

Role of MyD88 signaling in the imiquimod-induced mouse model of psoriasis: focus on innate myeloid cells.

Sara Costa, Olivia Marini, Dalila Bevilacqua, Anthony L DeFranco, Baidong Hou, Silvia Lonardi, William Vermi, Pamela Rodegher, Anna Panato, Franco Tagliaro and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Tm4sf19 inhibition alleviates imiquimod-induced psoriatic dermatitis by regulating inflammatory signaling pathways and keratinocyte proliferation in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  4. Discovery of IRAK4 InhibitorsJournal of medicinal chemistry · 2024
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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

14 authors at 4 institutions in 3 countries.

Sara CostaDepartment of Medicine, Division of General Pathology, University of Verona, Verona, Italy.
Olivia MariniDepartment of Medicine, Division of General Pathology, University of Verona, Verona, Italy.
Dalila BevilacquaDepartment of Medicine, Division of General Pathology, University of Verona, Verona, Italy.
Anthony L DeFrancoDepartment of Microbiology and Immunology, University of California, San Francisco, California, USA.
Baidong HouKey Laboratory of Infection and Immunity, Institute of Biophysics, Chaoyang District, Beijing, China.
Silvia LonardiDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
William VermiDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Pamela RodegherDepartment of Diagnostics and Public Health, Unit of Forensic Medicine, University of Verona, Verona, Italy.
Anna PanatoDepartment of Diagnostics and Public Health, Unit of Forensic Medicine, University of Verona, Verona, Italy.
Franco TagliaroDepartment of Diagnostics and Public Health, Unit of Forensic Medicine, University of Verona, Verona, Italy.
Clifford A LowellDepartment of Laboratory Medicine, University of California, San Francisco, California, USA; and.
Marco A CassatellaDepartment of Medicine, Division of General Pathology, University of Verona, Verona, Italy.
Giampiero GirolomoniDivision of Dermatology and Venereology, and University of Verona, Verona, Italy.
Patrizia ScapiniDepartment of Medicine, Division of General Pathology, University of Verona, Verona, Italy; patrizia.scapini@univr.it.
University of Verona · ITUniversity of Brescia · ITUniversity of California, San Francisco · USInstitute of Biophysics · CN

Funding

The contribution of innate immune cells to autoimmunityP01AI078869 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2008 to 2012
$8.9M
Regulation of Innate Immune Signaling by Lyn KinaseR01AI113272 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2015 to 2019
$2.0M
NIAID NIH HHS P01 AI078869NIAID NIH HHS R01 AI113272
6 · The paper itself

Abstract

Psoriasis is a chronic skin disease associated with deregulated activation of immune cells and keratinocytes. In this study, we used the imiquimod (IMQ)-induced mouse model of psoriasis to dissect better the contribution of hematopoietic and skin-resident stromal cells to psoriasis development. The comparison of disease development in mice carrying the hematopoietic cell-specific deletion of MyD88 (

Indexed as

AminoquinolinesAnimalsDisease Models, AnimalImiquimodImmunity, InnateInterleukin-1betaInterleukin-23MiceMice, KnockoutMyeloid CellsMyeloid Differentiation Factor 88PsoriasisSkinAminoquinolinesIL1B protein, mouseImiquimodInterleukin-1betaInterleukin-23Myd88 protein, mouseMyeloid Differentiation Factor 88monocytes/macrophagesneutrophilsskin inflammation

Identifiers

PMID28642279
PMCPMC6608051
OpenAlexW2700205502

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.