Evidence map›Paper›PMID 26994905›Full record

ArticleJournal of autoimmunity2016

Nanovesicle-targeted Kv1.3 knockdown in memory T cells suppresses CD40L expression and memory phenotype.

Ameet A Chimote, Peter Hajdu, Leah C Kottyan, John B Harley, Yeoheung Yun, Laura Conforti

Open access · greenAbstract read
In one paragraph

Article in Journal of autoimmunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Activity of Potassium Channels in CD8International journal of molecular sciences · 2024
    Article
  2. Article
  3. Review
  4. Review
  5. Targeted knockdown of the adenosine AMolecular therapy. Methods & clinical development · 2021
    Article
  6. Immune Checkpoint Inhibitors Regulate KFrontiers in pharmacology · 2021
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. 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 2 institutions in 1 country.

Ameet A ChimoteDepartment of Internal Medicine, Division of Nephrology, University of Cincinnati, Cincinnati, OH, USA.
Peter HajduDepartment of Internal Medicine, Division of Nephrology, University of Cincinnati, Cincinnati, OH, USA.
Leah C KottyanCenter for Autoimmune Genomics and Etiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
John B HarleyCenter for Autoimmune Genomics and Etiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA; US Department of Veterans Affairs Medical Center, Cincinnati, OH, USA.
Yeoheung YunNorth Carolina A & T State University, Chemical, Biological and Bioengineering Department, Greensboro, NC, USA.
Laura ConfortiDepartment of Internal Medicine, Division of Nephrology, University of Cincinnati, Cincinnati, OH, USA. Electronic address: Laura.Conforti@uc.edu.
University of Cincinnati · USNorth Carolina Agricultural and Technical State University · US

Funding

ROLE OF ANGPTL4, AN ANGIOGENIC MEDIATOR, IN ARTHRITISP30AR047363 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI FLICK, MATTHEW J. · 2001 to 2015
$9.2M
Tissue Repository CoreP30AR070549 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI Leah Claire Kottyan · 2016 to 2026
$7.7M
Hypoxia and Potassium Channel Activity in T LymphocytesR01CA095286 · NCI · UNIVERSITY OF CINCINNATI · PI CONFORTI, LAURA · 2003 to 2019
$4.1M
Targeted Ion Channel Downregulation By Nanoparticles: A Novel Therapeutic approaR21AR060966 · NIAMS · UNIVERSITY OF CINCINNATI · PI CONFORTI, LAURA · 2011 to 2012
$395k
NCI NIH HHS R01 CA095286NCI NIH HHS R01CA095286NIAMS NIH HHS R21 AR060966NIAMS NIH HHS R21AR060966
6 · The paper itself

Abstract

Ca(2+) signaling controls activation and effector functions of T lymphocytes. Ca(2+) levels also regulate NFAT activation and CD40 ligand (CD40L) expression in T cells. CD40L in activated memory T cells binds to its cognate receptor, CD40, on other cell types resulting in the production of antibodies and pro-inflammatory mediators. The CD40L/CD40 interaction is implicated in the pathogenesis of autoimmune disorders and CD40L is widely recognized as a therapeutic target. Ca(2+) signaling in T cells is regulated by Kv1.3 channels. We have developed lipid nanoparticles that deliver Kv1.3 siRNAs (Kv1.3-NPs) selectively to CD45RO(+) memory T cells and reduce the activation-induced Ca(2+) influx. Herein we report that Kv1.3-NPs reduced NFAT activation and CD40L expression exclusively in CD45RO(+) T cells. Furthermore, Kv1.3-NPs suppressed cytokine release and induced a phenotype switch of T cells from predominantly memory to naïve. These findings indicate that Kv1.3-NPs operate as targeted immune suppressive agents with promising therapeutic potentials.

Indexed as

Gene ExpressionGene Knockdown TechniquesImmunologic MemoryPhenotypeAdultAntigens, SurfaceCD40 LigandCytokinesFemaleHumansImmunophenotypingKv1.3 Potassium ChannelMiddle AgedNanoparticlesNFATC Transcription FactorsProtein TransportAntigens, SurfaceCD40 LigandCytokinesKv1.3 Potassium ChannelNFATC Transcription FactorsAutoimmunityCa(2+) signalingCD40 ligandKv1.3 ion channelLipid nanoparticlesT cell

Identifiers

PMID26994905
PMCPMC4830342
OpenAlexW2299085783

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.