Evidence map›Paper›PMID 24637841›Full record

ArticlePloS one2014

Reduced B lymphoid kinase (Blk) expression enhances proinflammatory cytokine production and induces nephrosis in C57BL/6-lpr/lpr mice.

Elizabeth M Samuelson, Renee M Laird, Amber M Papillion, Arthur H Tatum, Michael F Princiotta, Sandra M Hayes

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
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  12. The up-to-date pathophysiology of Kawasaki disease.Clinical & translational immunology · 2021
    Review
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  15. Article
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  17. Article
  18. Recent Advances in Defining the Genetic Basis of Rheumatoid Arthritis.Annual review of genomics and human genetics · 2016
    Review
  19. Review
  20. Review
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

6 authors at 1 institution in 1 country.

Elizabeth M SamuelsonDepartment of Microbiology and Immunology, State University of New York Upstate Medical University, Syracuse, New York, United States of America.
Renee M LairdDepartment of Microbiology and Immunology, State University of New York Upstate Medical University, Syracuse, New York, United States of America.
Amber M PapillionDepartment of Microbiology and Immunology, State University of New York Upstate Medical University, Syracuse, New York, United States of America.
Arthur H TatumDepartment of Pathology, State University of New York Upstate Medical University, Syracuse, New York, United States of America.
Michael F PrinciottaDepartment of Microbiology and Immunology, State University of New York Upstate Medical University, Syracuse, New York, United States of America.
Sandra M HayesDepartment of Microbiology and Immunology, State University of New York Upstate Medical University, Syracuse, New York, United States of America.
SUNY Upstate Medical University · US

Funding

Blk as a Master Regulator of Marginal Zone B Cell Development and ActivationR21AI097694 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI HAYES, SANDRA MARIE · 2012 to 2013
$424k
Role of B Lymphoid Kinase in the Development of SLER56AI091908 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI HAYES, SANDRA MARIE · 2011 to 2011
$395k
NIAID NIH HHS R21 AI097694NIAID NIH HHS R56 AI091908
6 · The paper itself

Abstract

BLK, which encodes B lymphoid kinase, was recently identified in genome wide association studies as a susceptibility gene for systemic lupus erythematosus (SLE), and risk alleles mapping to the BLK locus result in reduced gene expression. To determine whether BLK is indeed a bona fide susceptibility gene, we developed an experimental mouse model, namely the Blk+/-.lpr/lpr (Blk+/-.lpr) mouse, in which Blk expression levels are reduced to levels comparable to those in individuals carrying a risk allele. Here, we report that Blk is expressed not only in B cells, but also in IL-17-producing γδ and DN αβ T cells and in plasmacytoid dendritic cells (pDCs). Moreover, we found that solely reducing Blk expression in C57BL/6-lpr/lpr mice enhanced proinflammatory cytokine production and accelerated the onset of lymphoproliferation, proteinuria, and kidney disease. Together, these findings suggest that BLK risk alleles confer susceptibility to SLE through the dysregulation of a proinflammatory cytokine network.

Indexed as

AnimalsAutoimmune DiseasesB-LymphocytesCell CountCytokinesDendritic CellsImmune ToleranceInducible T-Cell Co-Stimulator LigandInducible T-Cell Co-Stimulator ProteinInflammation MediatorsKidneyMacrophagesMiceMice, Inbred C57BLMice, Inbred MRL lprMice, TransgenicB lymphoid kinase, mouseCytokinesIcosl protein, mouseIcos protein, mouseInducible T-Cell Co-Stimulator LigandInducible T-Cell Co-Stimulator ProteinInflammation MediatorsReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltasrc-Family Kinases

Identifiers

PMID24637841
PMCPMC3956874
OpenAlexW2033414663

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.