Evidence map›Paper›PMID 17100774›Full record

ArticleClinical and experimental immunology2006

Atorvastatin interferes with activation of human CD4(+) T cells via inhibition of small guanosine triphosphatase (GTPase) activity and caspase-independent apoptosis.

P-T Brinkkoetter, U Gottmann, J Schulte, F J van der Woude, C Braun, B A Yard

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

17 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Observational
  4. Review
  5. Article
  6. Pitavastatin Is a Highly Potent Inhibitor of T-Cell Proliferation.Pharmaceuticals (Basel, Switzerland) · 2021
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Statin use and ocular inflammatory disease risk.Journal of ophthalmic inflammation and infection · 2013
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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.

P-T BrinkkoetterV. Department of Medicine (Nephrology), University Hospital Mannheim, University of Heidelberg, Germany.
U Gottmann
J Schulte
F J van der Woude
C Braun
B A Yard
Heidelberg University · DEUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although a beneficial effect of hydroxy-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, i.e. statins, on cell-mediated immunity has been suggested in vivo and in vitro, little is known about the molecular and biochemical events by which statins inhibit T cell proliferation. To address this question, we investigated the effects of atorvastatin (AT) on intracellular cytokine production, T cell activation markers, cell cycle progression and apoptosis in human CD4(+) T cells. AT did not influence intracellular cytokine production after short-term stimulation of whole blood with phorbol myristate acetate (PMA)/ionomycin or superantigen (SEB). In contrast, AT influenced CD45RA to RO switching dose-dependently, as well as CD25 expression, and caused cell cycle arrest in the G1 phase after long-term T cell stimulation. This occurred in conjunction with a reduced expression of cyclin-dependent kinases 2 and 4 and p21(wav1/cip1) and was paralleled by an increased protein expression of p27(kip1). In addition to G1 arrest, increased apoptosis was observed in AT-treated cells. In line with this, the expression of Bcl-xl and pBad were decreased by AT. Apoptosis was independent of caspases 3 and 9 activation. The inhibitory effect of AT on T cell proliferation could be overcome by addition of mevalonic acid or geranylgeranyl pyrophosphate, but not by farnesyl pyrophosphate or squalen, suggesting reduced protein prenylation. Activation of Rho, Rac and Ras were strongly reduced in AT-treated T cells, suggesting that impaired geranylation of these molecules might underlie the inhibitory effect of AT on T cell proliferation.

Indexed as

ApoptosisAtorvastatinBlotting, WesternCaspasesCD4-Positive T-LymphocytesCell CycleCell ProliferationCytokinesDose-Response Relationship, ImmunologicEnzyme ActivationHeptanoic AcidsHumansHydroxymethylglutaryl-CoA Reductase InhibitorsInterleukin-2 Receptor alpha SubunitLymphocyte ActivationMonomeric GTP-Binding ProteinsAtorvastatinCaspasesCytokinesHeptanoic AcidsHydroxymethylglutaryl-CoA Reductase InhibitorsInterleukin-2 Receptor alpha SubunitMonomeric GTP-Binding ProteinsPyrroles

Identifiers

PMID17100774
PMCPMC1810423
OpenAlexW1988837216

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.