Evidence map›Paper›PMID 27781323›Full record

ArticleScandinavian journal of immunology2016

Therapeutic Potential for Targeting the Suppressor of Cytokine Signalling-1 Pathway for the Treatment of SLE.

B Sukka-Ganesh, J Larkin

Open access · greenAbstract read
In one paragraph

Article in Scandinavian journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 22 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

2 authors at 1 institution in 1 country.

B Sukka-GaneshDepartment of Microbiology and Cell Science, University of Florida, Gainesville, FL, USA.
J LarkinDepartment of Microbiology and Cell Science, University of Florida, Gainesville, FL, USA. jlarkin3@ufl.edu.
University of Florida · US

Funding

Using social networks to map and evaluate team science across CTSA hubsUL1TR001427 · NCATS · UNIVERSITY OF FLORIDA · PI MITCHELL, DUANE A. · 2015 to 2024
$37.2M
UF Clinical and Translational Science AwardUL1TR000064 · NCATS · UNIVERSITY OF FLORIDA · PI NELSON, DAVID R · 2012 to 2014
$12.2M
Defining the role of altered cytokine signaling pathways on autoimmunityU01AI101990 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2012 to 2016
$12.1M
UF Clinical and Translational Science AwardTL1TR000066 · NCATS · UNIVERSITY OF FLORIDA · PI NELSON, DAVID R · 2012 to 2014
$345k
NCATS NIH HHS TL1 TR000066NCATS NIH HHS UL1 TR000064NCATS NIH HHS UL1 TR001427NIAID NIH HHS U01 AI101990
6 · The paper itself

Abstract

Although the specific events dictating systemic lupus erythematosus (SLE) pathology remain unclear, abundant evidence indicates a critical role for dysregulated cytokine signalling in disease progression. Notably, the suppressor of cytokine signalling (SOCS) family of intracellular proteins, in particular the kinase inhibitory region (KIR) bearing SOCS1 and SOCS3, plays a critical role in regulating cytokine signalling. To assess a relationship between SOCS1/SOCS3 expression and SLE, the goals of this study were to (1) evaluate the time kinetics of SOCS1/SOCS3 message and protein expression based on SLE-associated stimulations, (2) compare levels of SOCS1 and SOCS3 present in SLE patients and healthy controls by message and protein, (3) relate SOCS1/SOCS3 expression to inflammatory markers in SLE patients and (4) correlate SOCS1/SOCS3 levels to current treatments. We found that SOCS1 and SOCS3 were most abundant in murine splenic samples at 48 h subsequent to stimulation by anti-CD3, LPS or interferon-gamma. In addition, significant reductions in SOCS1 and SOCS3 were present within PMBCs of SLE patients compared to controls by both mRNA and protein expression. We also found that decreased levels of SOCS1 in SLE patients were correlated with enhanced levels of inflammatory markers and upregulated expression of MHC class II. Finally, we show that patients receiving steroid treatment possessed higher levels SOCS1 compared to SLE patient counterparts and that steroid administration to human PBMCs upregulated SOCS1 message in a dose- and time-dependent manner. Together, these results suggest that therapeutic strategies focused on SOCS1 signalling may have efficacy in the treatment of SLE.

Indexed as

AdolescentAdultAgedAnimalsAntibodiesAnti-Inflammatory AgentsCase-Control StudiesCD3 ComplexFemaleGene Expression RegulationHistocompatibility Antigens Class IIHumansInterferon-gammaLeukocytes, MononuclearLipopolysaccharidesLupus Erythematosus, SystemicAntibodiesAnti-Inflammatory AgentsCD3 ComplexHistocompatibility Antigens Class IIInterferon-gammaLipopolysaccharidesRNA, MessengerSOCS1 protein, humanSOCS3 protein, humanSTAT1 protein, humanSTAT1 Transcription FactorSteroidsSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling 3 Protein

Identifiers

PMID27781323
PMCPMC5131794
OpenAlexW2544456119

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.