Evidence map›Paper›PMID 17495133›Full record

Trial reportBlood2007

The unexpected effect of cyclosporin A on CD56+CD16- and CD56+CD16+ natural killer cell subpopulations.

Hongbo Wang, Bartosz Grzywacz, David Sukovich, Valarie McCullar, Qing Cao, Alisa B Lee, Bruce R Blazar, David N Cornfield, Jeffrey S Miller, Michael R Verneris

Open access · bronzeAbstract readClinical TrialComparative Study
In one paragraph

Trial report in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 136 citations in OpenAlex.

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  18. Review
  19. Distinct Effects of Immunosuppressive Drugs on the Anti-Pathogens (Basel, Switzerland) · 2019
    Article
  20. Biological effects of cyclosporin A on CD3Molecular and cellular biochemistry · 2019
    Article

1 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Hongbo WangDepartment of Pediatrics, Cancer Center, University of Minnesota, Minneapolis, USA.
Bartosz Grzywacz
David Sukovich
Valarie McCullar
Qing Cao
Alisa B Lee
Bruce R Blazar
David N Cornfield
Jeffrey S Miller
Michael R Verneris
Stanford University · USUniversity of Minnesota · US

Funding

Trial Design and Biostatistical Support CoreP01CA065493 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Mark J Osborn · 1995 to 2026
$48.2M
IN VIVO PREVENTION OF MURINE GVHDR01AI034495 · NIAID · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BLAZAR, BRUCE R · 1993 to 2016
$6.2M
GVL TO REDUCE AML RELAPSE AFTER MURINE ALLOGENEIC BMTR01CA072669 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BLAZAR, BRUCE R · 1997 to 2017
$4.9M
NK Cell Differentiation from Stem CellsR01HL055417 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI MILLER, JEFFREY S. · 2000 to 2010
$3.2M
ACTIVITY OF EXPANDED GAMMA/DELTA T CELLSK08HL004505 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI VERNERIS, MICHAEL R · 2001 to 2005
$622k
NCI NIH HHS P01 CA065493NCI NIH HHS P01 CA65493NCI NIH HHS R01 CA072669NCI NIH HHS R01 CA72669NHLBI NIH HHS K08 HL004505NHLBI NIH HHS K08 HL04505-03NHLBI NIH HHS R01 HL055417NHLBI NIH HHS R01 HL55417NIAID NIH HHS R01 AI034495NIAID NIH HHS R01 AI34495
6 · The paper itself

Abstract

Cyclosporin A (CSA) is commonly used to prevent graft-versus-host disease. The influence of CSA on T-cell function has been extensively investigated; however, the effect of CSA on natural killer (NK) cells is less understood. NK cells were cultured with IL-2 and IL-15 with and without CSA for 1 week. Compared with controls, CSA-treated cultures showed fewer CD56(+)CD16(+)KIR(+) NK cells and a reciprocal increase in CD56(+)CD16(-)KIR(-) cells. These changes were due mainly to a reduced proliferation of the CD56(dim) NK-cell subpopulation and a relative resistance of CD56(bright) NK cells to CSA. Following coculture with K562 targets, CSA-exposed NK cells differed from controls and lacked Ca(2+) oscillations, nuclear factor of activated T cells (NFAT) dephosphorylation, and NFAT nuclear translocation. NK cells cultured in CSA retained cytotoxicity against K562, Raji, and KIR ligand-expressing lymphoblastoid cells. NK cells cultured in CSA showed increases in NKp30 and reductions in NKp44 and NKG2D. Following IL-12 and IL-18 stimulation, CSA-treated NK cells showed more IFN-gamma-producing cells. Using in vitro NK-cell differentiation, progenitor cells gave rise to more CD56(+)KIR(-) NK cells in the presence of CSA than controls. Collectively, these studies show that CSA influences NK-cell function and phenotype, which may have important implications for graft-versus-leukemia effects.

Indexed as

Antigens, CDCD56 AntigenReceptors, IgGActive Transport, Cell NucleusCalcium SignalingCell DifferentiationCell NucleusCell ProliferationCoculture TechniquesCyclosporineCytokinesGPI-Linked ProteinsGraft vs Host DiseaseGraft vs Leukemia EffectHumansImmunosuppressive AgentsAntigens, CDCD56 AntigenCyclosporineCytokinesFCGR3B protein, humanGEM protein, humanGPI-Linked ProteinsImmunosuppressive AgentsMonomeric GTP-Binding ProteinsNFATC Transcription FactorsReceptors, IgG

Identifiers

PMID17495133
PMCPMC1975839
OpenAlexW1965982369

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.