Evidence map›Paper›PMID 21107834›Full record

ArticleCancer immunology, immunotherapy : CII2011

Rapamycin increases the yield and effector function of human γδ T cells stimulated in vitro.

Haishan Li, C David Pauza

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

32 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
  2. γδ T cells and cancer.The Journal of clinical investigation · 2026
    Review
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  10. The immunomodulatory effects of endocrine therapy in breast cancer.Journal of experimental & clinical cancer research : CR · 2021
    Review
  11. Review
  12. Article
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  15. Review
  16. Bordeaux 2018: Wine, Cheese, and γδ T Cells.Frontiers in immunology · 2019
    Article
  17. Review
  18. Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Haishan LiInstitute of Human Virology, University of Maryland School of Medicine, 725 W. Lombard St. Rm. N546, Baltimore, MD 21201, USA.
C David Pauza
University of Maryland, Baltimore · US

Funding

Mechanisms for depleting tumor immunity in AIDSR01CA142458 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI PAUZA, C. DAVID · 2009 to 2012
$1.6M
NCI NIH HHS CA142458NCI NIH HHS R01 CA142458
6 · The paper itself

Abstract

Clinical strategies to exploit Vγ2Vδ2 T cell responses for immunotherapy are confronted with short-term increases in cell levels or activity and the development of anergy that reduces the response to therapy with succeeding treatments. We are exploring strategies to increase the yield and durability of elicited Vγ2Vδ2 T cell responses. One approach focuses on the mammalian target of rapamycin (mTOR), which is important for regulating T cell metabolism and function. In Vγ2Vδ2 T cells, mTOR phosphorylates the S6K1 and eIF4EBP1 signaling intermediates after antigen stimulation. Rapamycin inhibited these phosphorylation events without impacting Akt or Erk activation, even though specific inhibition of Akt or Erk in turn reduced the activation of mTOR. The effects of rapamycin on the T cell receptor signaling pathway lead to increased proliferation of treated and antigen-exposed Vγ2Vδ2 cells. Rapamycin altered the phenotype of antigen-specific Vγ2Vδ2 cells by inducing a population shift from CD62L + CD69- to CD62L-CD69+, higher expression of CD25 or Bcl-2, lower levels of CCR5 and increased resistance to Fas-mediated cellular apoptosis. These changes were consistent with rapamycin promoting cell activation while decreasing the susceptibility to cell death that might occur by CCR5 or Fas signaling. Rapamycin treatment during antigen-stimulation of Vγ2Vδ2 T cells may be a strategy for overcoming current obstacles in tumor immunotherapy.

Indexed as

Antibiotics, AntineoplasticAntigen-Presenting CellsApoptosisCell Line, TumorCell ProliferationFlow CytometryGene Expression Regulation, NeoplasticHumansInterleukin-2 Receptor alpha SubunitIn Vitro TechniquesLymphocyte ActivationProto-Oncogene Proteins c-bcl-2Receptors, Antigen, T-Cell, gamma-deltaReceptors, CCR5Signal TransductionSirolimusAntibiotics, AntineoplasticIL2RA protein, humanInterleukin-2 Receptor alpha SubunitMTOR protein, humanProto-Oncogene Proteins c-bcl-2Receptors, Antigen, T-Cell, gamma-deltaReceptors, CCR5SirolimusTOR Serine-Threonine Kinases

Identifiers

PMID21107834
PMCPMC3077899
OpenAlexW2066937567

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.