Evidence map›Paper›PMID 22661089›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Myeloid dendritic cells from B6.NZM Sle1/Sle2/Sle3 lupus-prone mice express an IFN signature that precedes disease onset.

Uma Sriram, Linda Varghese, Heather L Bennett, Neelakshi R Jog, Debra K Shivers, Yue Ning, Edward M Behrens, Roberto Caricchio, Stefania Gallucci

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. 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
2.8field-weighted citation impact, top 11% 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, 45 citations in OpenAlex.

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  11. Metformin Inhibits the Type 1 IFN Response in Human CD4Journal of immunology (Baltimore, Md. : 1950) · 2019
    Article
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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

9 authors at 2 institutions in 1 country.

Uma SriramLaboratory of Dendritic Cell Biology, Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140, USA. sriram@temple.edu
Linda Varghese
Heather L Bennett
Neelakshi R Jog
Debra K Shivers
Yue Ning
Edward M Behrens
Roberto Caricchio
Stefania Gallucci
Temple University · USChildren's Hospital of Philadelphia · US

Funding

Regulation of Type I IFNs in Tolerance and AutoimmunityR01AI076423 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI GALLUCCI, STEFANIA · 2009 to 2013
$1.7M
NIAID NIH HHS R01 AI076423NIAID NIH HHS R01-AI076423
6 · The paper itself

Abstract

Patients with systemic lupus erythematosus show an overexpression of type I IFN-responsive genes that is referred to as "IFN signature." We found that B6.NZMSle1/Sle2/Sle3 (Sle1,2,3) lupus-prone mice also express an IFN signature compared with non-autoimmune C57BL/6 mice. In vitro, myeloid dendritic cells (mDCs) (GM-CSF bone marrow-derived dendritic cells; BMDCs) from Sle1,2,3 mice constitutively overexpressed IFN-responsive genes such as IFN-β, Oas-3, Mx-1, ISG-15, and CXCL10 and members of the IFN signaling pathway STAT1, STAT2, and IRF7. The IFN signature was similar in Sle1,2,3 BMDCs from young, pre-autoimmune mice and from mice with high titers of autoantibodies, suggesting that the IFN signature in mDCs precedes disease onset and is independent from the autoantibodies. Sle1,2,3 BMDCs hyperresponded to stimulation with IFN-α and the TLR7 and TLR9 agonists R848 and CpGs. We propose that this hyperresponse is induced by the IFN signature and only partially contributes to the signature, as oligonucleotides inhibitory for TLR7 and TLR9 only partially suppressed the constitutive IFN signature, and pre-exposure to IFN-α induced the same hyperresponse in wild-type BMDCs as in Sle1,2,3 BMDCs. In vivo, mDCs and to a lesser extent T and B cells from young prediseased Sle1,2,3 mice also expressed the IFN signature, although they lacked the strength that BMDCs showed in vitro. Sle1,2,3 plasmacytoid DCs expressed the IFN signature in vitro but not in vivo, suggesting that mDCs may be more relevant before disease onset. We propose that Sle1,2,3 mice are useful tools to study the role of the IFN signature in lupus pathogenesis.

Indexed as

AnimalsAutoantibodiesCells, CulturedCellular SenescenceDisease Models, AnimalFemaleGene Expression RegulationGenetic Predisposition to DiseaseInterferonsLupus Erythematosus, SystemicMaleMiceMice, Inbred C57BLMice, Inbred NZBMyeloid CellsTime FactorsAutoantibodiesInterferons

Identifiers

PMID22661089
PMCPMC3381850
OpenAlexW1936067328

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.