Evidence map›Paper›PMID 21282105›Full record

ArticleThe Journal of biological chemistry2011

Minocycline suppresses activation of nuclear factor of activated T cells 1 (NFAT1) in human CD4+ T cells.

Gregory L Szeto, Joel L Pomerantz, David R M Graham, Janice E Clements

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Antibiotics for Rheumatologic Diseases: A Critical Review.International journal of molecular sciences · 2025
    Review
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  4. Article
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  10. Article
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  12. Article
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  14. Opinion: An Existing Drug to AssessFrontiers in pharmacology · 2019
    Article
  15. Article
  16. Article
  17. Activation of the TXNIP/NLRP3 inflammasome pathway contributes to inflammation in diabetic retinopathy: a novel inhibitory effect of minocycline.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Article
  18. Article
  19. Review
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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 1 institution in 1 country.

Gregory L SzetoDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Joel L Pomerantz
David R M Graham
Janice E Clements
Johns Hopkins Medicine · US

Funding

Minocycline Inhibits Immune Reactivation of CNS SIVR01NS055648 · NINDS · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE E · 2007 to 2011
$3.2M
Minocycline Immune Effects on SIV CNS DiseaseR01MH087233 · NIMH · JOHNS HOPKINS UNIVERSITY · PI GRAHAM, DAVID R. M., ZINK, M CHRISTINE · 2010 to 2014
$3.0M
NIMH NIH HHS MH087233NIMH NIH HHS R01 MH087233NINDS NIH HHS NS055648NINDS NIH HHS R01 NS055648
6 · The paper itself

Abstract

Minocycline is a tetracycline family antibiotic that has anti-inflammatory and immunomodulatory properties. These properties have shown promise in the treatment of conditions such as rheumatoid arthritis, Huntington disease, and multiple sclerosis. As lymphocyte activation is involved in the pathogenesis of many of these diseases, T cells are postulated to be a primary target in minocycline therapy. Previous studies have demonstrated attenuation of CD4(+) T cell activation by minocycline, but a specific mechanism has not been elucidated. In this study, we investigated the effect of minocycline on the activity of three key transcription factors regulating CD4(+) T cell activation: NF-κB, AP-1 (activator protein 1), and NFAT (nuclear factor of activated T) cells. Our data demonstrate that minocycline selectively impairs NFAT-mediated transcriptional activation, a result of increased phosphorylation and reduced nuclear translocation of the isoform NFAT1. Minocycline increased the activity of the NFAT kinase GSK3 and decreased intracellular Ca(2+) flux, both of which facilitate NFAT1 phosphorylation. These findings provide a novel mechanism for minocycline induced suppression of CD4(+) T cell activation and may better inform the application of minocycline as an immunomodulatory agent.

Indexed as

Active Transport, Cell NucleusAnti-Bacterial AgentsAnti-Inflammatory AgentsArthritis, RheumatoidCalcium SignalingCD4-Positive T-LymphocytesCell NucleusCells, CulturedEnzyme ActivationEnzyme ActivatorsGlycogen Synthase Kinase 3HumansHuntington DiseaseLymphocyte ActivationMinocyclineMultiple SclerosisAnti-Bacterial AgentsAnti-Inflammatory AgentsEnzyme ActivatorsGlycogen Synthase Kinase 3MinocyclineNFATC2 protein, humanNFATC Transcription FactorsNF-kappa BProtein IsoformsTranscription Factor AP-1

Identifiers

PMID21282105
PMCPMC3064183
OpenAlexW2106758558

What OpenQuestion holds

Textmetadata
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.