Evidence map›Paper›PMID 22581856›Full record

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

Kv1.3 deletion biases T cells toward an immunoregulatory phenotype and renders mice resistant to autoimmune encephalomyelitis.

Anne R Gocke, Lori A Lebson, Inna V Grishkan, Lina Hu, Hai M Nguyen, Katharine A Whartenby, K George Chandy, Peter A Calabresi

Open access · bronzeAbstract read
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 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.2field-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

47 citing papers in PubMed, 72 citations in OpenAlex.

  1. Trial
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  3. Identification of Novel Kv1.3 Channel-Interacting Proteins Using Proximity Labelling in T-Cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2025
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  20. Dlg1 Maintains Dendritic Cell Function by Securing Voltage-Gated KJournal of immunology (Baltimore, Md. : 1950) · 2019
    Article
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

8 authors at 3 institutions in 1 country.

Anne R GockeDepartment of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. agocke4@jhu.edu
Lori A Lebson
Inna V Grishkan
Lina Hu
Hai M Nguyen
Katharine A Whartenby
K George Chandy
Peter A Calabresi
Johns Hopkins Medicine · USJohns Hopkins University · USUniversity of California, Irvine · US

Funding

The Role of KV1.3 in Effector T cellsR01NS041435 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI CALABRESI, PETER A · 2000 to 2025
$5.8M
NINDS NIH HHS R01 NS041435NINDS NIH HHS R01NS041435
6 · The paper itself

Abstract

Increasing evidence suggests ion channels have critical functions in the differentiation and plasticity of T cells. Kv1.3, a voltage-gated K(+) channel, is a functional marker and a pharmacological target for activated effector memory T cells. Selective Kv1.3 blockers have been shown to inhibit proliferation and cytokine production by human and rat effector memory T cells. We used Kv1.3 knockout (KO) mice to investigate the mechanism by which Kv1.3 blockade affects CD4(+) T cell differentiation during an inflammatory immune-mediated disease. Kv1.3 KO animals displayed significantly lower incidence and severity of myelin oligodendrocyte glycoprotein (MOG) peptide-induced experimental autoimmune encephalomyelitis. Kv1.3 was the only K(V) channel expressed in MOG 35-55-specific CD4(+) T cell blasts, and no K(V) current was present in MOG-specific CD4(+) T cell-blasts from Kv1.3 KO mice. Fewer CD4(+) T cells migrated to the CNS in Kv1.3 KO mice following disease induction, and Ag-specific proliferation of CD4(+) T cells from these mice was impaired with a corresponding cell-cycle delay. Kv1.3 was required for optimal expression of IFN-γ and IL-17, whereas its absence led to increased IL-10 production. Dendritic cells from Kv1.3 KO mice fully activated wild-type CD4(+) T cells, indicating a T cell-intrinsic defect in Kv1.3 KO mice. The loss of Kv1.3 led to a suppressive phenotype, which may contribute to the mechanism by which deletion of Kv1.3 produces an immunotherapeutic effect. Skewing of CD4(+) T cell differentiation toward Ag-specific regulatory T cells by pharmacological blockade or genetic suppression of Kv1.3 might be beneficial for therapy of immune-mediated diseases such as multiple sclerosis.

Indexed as

AnimalsBlotting, WesternCD4-Positive T-LymphocytesCell DifferentiationElectrophysiologyEncephalomyelitis, Autoimmune, ExperimentalEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryKv1.3 Potassium ChannelLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicPhenotypeKv1.3 Potassium Channel

Identifiers

PMID22581856
PMCPMC3370138
OpenAlexW2123879187

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.