Evidence map›Paper›PMID 23542035›Full record

ArticleFEBS letters2013

IFNβ autocrine feedback is required to sustain TLR induced production of MCP-1 in macrophages.

Michael J Pattison, Kirsty F MacKenzie, Suzanne E Elcombe, J Simon C Arthur

Open access · hybridAbstract read
In one paragraph

Article in FEBS letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

22 citing papers in PubMed, 26 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Michael J PattisonMRC Protein Phosphorylation Unit, Wellcome Trust Building, College of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland.
Kirsty F MacKenzie
Suzanne E Elcombe
J Simon C Arthur
MRC Protein Phosphorylation and Ubiquitylation Unit · GBUniversity of Dundee · GB

Funding

Medical Research Council MC_U127081014Medical Research Council MC_UU_12016/10Wellcome TrustWellcome Trust 087079/Z/08/Z
6 · The paper itself

Abstract

Chemokines, including MCP-1, are crucial to mounting an effective immune response due to their ability to recruit other immune cells. We show that sustained LPS or poly(I:C)-stimulated MCP-1 production requires an IFNβ-mediated feedback loop. Consistent with this, exogenous IFNβ was able to induce MCP-1 transcription in the absence of other stimuli. Blocking IFNβ signaling with Ruxolitinib, a JAK inhibitor, inhibited MCP-1 transcription. The MCP-1 promoter contains potential STAT binding sites and we demonstrate that STAT1 is recruited upon IFNβ stimulation. Furthermore we find that IL-10 knockout increases MCP-1 production in response to LPS, which may reflect an ability of IL-10 to repress IFNβ production. Overall, these results show the importance of the balance between IFNβ and IL-10 in the regulation of MCP-1.

Indexed as

AnimalsAutocrine CommunicationCells, CulturedChemokine CCL2Feedback, PhysiologicalInterferon-betaInterleukin-10MacrophagesMiceMice, Inbred C57BLMice, KnockoutReceptor, Interferon alpha-betaToll-Like ReceptorsUp-RegulationCcl2 protein, mouseChemokine CCL2Interferon-betaInterleukin-10Receptor, Interferon alpha-betaToll-Like Receptors

Identifiers

PMID23542035
PMCPMC3655261
OpenAlexW2033135715

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.