Evidence map›Paper›PMID 25936433›Full record

ArticleMolecular medicine reports2015

Enhancement of the antigen-specific cytotoxic T lymphocyte-inducing ability in the PMDC11 leukemic plasmacytoid dendritic cell line via lentiviral vector-mediated transduction of the caTLR4 gene.

Minami Iwabuchi, Miwako Narita, Takayoshi Uchiyama, Shunpei Iwaya, Eri Oiwa, Yoshinori Nishizawa, Shigeo Hashimoto, Aude Bonehill, Noriyuki Kasahara, Jun Takizawa and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 47% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

11 authors at 4 institutions in 3 countries.

Minami IwabuchiLaboratory of Hematology and Oncology, Graduate School of Health Sciences, Niigata University, Nagaoka, Niigata 951‑8518, Japan.
Miwako NaritaLaboratory of Hematology and Oncology, Graduate School of Health Sciences, Niigata University, Nagaoka, Niigata 951‑8518, Japan.
Takayoshi UchiyamaLaboratory of Hematology and Oncology, Graduate School of Health Sciences, Niigata University, Nagaoka, Niigata 951‑8518, Japan.
Shunpei IwayaLaboratory of Hematology and Oncology, Graduate School of Health Sciences, Niigata University, Nagaoka, Niigata 951‑8518, Japan.
Eri OiwaLaboratory of Hematology and Oncology, Graduate School of Health Sciences, Niigata University, Nagaoka, Niigata 951‑8518, Japan.
Yoshinori NishizawaLaboratory of Hematology and Oncology, Graduate School of Health Sciences, Niigata University, Nagaoka, Niigata 951‑8518, Japan.
Shigeo HashimotoDivision of Hematology, Nagaoka Red Cross Hospital, Nagaoka, Niigata 951‑8518, Japan.
Aude BonehillLaboratory of Cellular and Molecular Therapy, Department of Physiology and Immunology, Medical School of the Free University Brussels (VUB), Laarbeeklaan 103, 1090 Brussels, Belgium.
Noriyuki KasaharaCURE Vector Core & JCCC Vector Shared Resource Facility, University of California, Los Angeles, CA 90095, USA.
Jun TakizawaDivision of Hematology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, Niigata University, Niigata 951‑8510, Japan.
Masuhiro TakahashiLaboratory of Hematology and Oncology, Graduate School of Health Sciences, Niigata University, Nagaoka, Niigata 951‑8518, Japan.
Niigata University · JPNagaoka Red Cross Hospital · JPVector (United States) · USVrije Universiteit Brussel · BE

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
PREVENTIVE ONCOLOGY ACADEMIC AWARDK07CA001604 · NCI · GEORGETOWN UNIVERSITY · PI LERMAN, CARYN · 1991 to 1995
–
NCI NIH HHS JCCC/P30 CA01604NCI NIH HHS P30 CA016042NIDDK NIH HHS CURE/P30 DK041301NIDDK NIH HHS P30 DK041301
6 · The paper itself

Abstract

The aim of the present study was to enhance the efficiency of leukemia immunotherapy by increasing the antigen-specific cytotoxic T lymphocyte-inducing ability of leukemia cells. The leukemic plasmacytoid dendritic cell line PMDC05 containing the HLA-A02/24 antigen, which was previously established in our laboratory (Laboratory of Hematology and Oncology, Graduate School of Health Sciences, Niigata University, Niigata, Japan), was used in the present study. It exhibited higher expression levels of CD80 following transduction with lentiviruses encoding the CD80 gene. This CD80-expressing PMDC05 was named PMDC11. In order to establish a more potent antigen-presenting cell for cellular immunotherapy of tumors or severe infections, PMDC11 cells were transduced with a constitutively active (ca) toll-like receptor 4 (TLR4) gene using the Tet-On system (caTLR4-PMDC11). CD8(+) T cells from healthy donors with HLA-A02 were co-cultured with mutant WT1 peptide-pulsed PMDC11, lipopolysaccharide (LPS)-stimulated PMDC11 or caTLR4-PMDC11 cells. Interleukin (IL)-2 (50 IU/ml) and IL-7 (10 ng/ml) were added on day three of culture. Priming with mutant WT1 peptide-pulsed PMDC11, LPS-stimulated PMDC11 or caTLR4-PMDC11 cells was conducted once per week and two thirds of the IL-2/IL-7 containing medium was replenished every 3-4 days. Immediately prior to the priming with these various PMDC11 cells, the cultured cells were analyzed for the secretion of interferon (IFN)-γ in addition to the percentage and number of CD8(+)/WT1 tetramer(+) T cells using flow cytometry. caTLR4-PMDC11 cells were observed to possess greater antigen-presenting abilities compared with those of PMDC11 or LPS-stimulated PMDC11 cells in a mixed leukocyte culture. CD8 T cells positive for the WT1 tetramer were generated following 3-4 weeks of culture and CD8(+)/WT1 tetramer+ T cells were markedly increased in caTLR4-PMDC11-primed CD8(+) T cell culture compared with PMDC11 or LPS-stimulated PMDC11-primed CD8(+) T cell culture. These CD8(+) T cells co-cultured with caTLR4-PMDC11 cells were demonstrated to secrete IFN-γ and to be cytotoxic to WT1-expressing target cells. These data suggested that the antigen-specific cytotoxic T lymphocyte (CTL)-inducing ability of PMDC11 was potentiated via transduction of the caTLR4 gene. The present study also suggested that caTLR4-PMDC11 cells may be applied as potent antigen-presenting cells for generating antigen-specific CTLs in adoptive cellular immunotherapy against tumors and severe viral infections.

Indexed as

Gene Expression Regulation, LeukemicTransduction, GeneticAntigen PresentationAntigens, NeoplasmB7-1 AntigenCell Line, TumorCoculture TechniquesDendritic CellsGenetic VectorsHLA-A AntigensHumansImmunotherapyInterferon-gammaInterleukin-2Interleukin-7LentivirusAntigens, NeoplasmB7-1 AntigenHLA-A AntigensIL7 protein, humanInterferon-gammaInterleukin-2Interleukin-7TLR4 protein, humanToll-Like Receptor 4WT1 Proteins

Identifiers

PMID25936433
PMCPMC4464268
OpenAlexW2078286955

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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.