Evidence map›Paper›PMID 19009294›Full record

ArticleCancer immunology, immunotherapy : CII2009

Chronic lymphocytic leukemia (CLL) cells genetically modified to express B7-1, ICAM-1, and LFA-3 confer APC capacity to T cells from CLL patients.

Mary T Litzinger, Kenneth A Foon, Helen Sabzevari, Kwong-Yok Tsang, Jeffrey Schlom, Claudia Palena

Abstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.1field-weighted citation impact, top 44% 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

6 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Immune gene therapy of cancerTurkish journal of medical sciences · 2020
    Review
  4. Review
  5. Article
  6. 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 4 institutions in 1 country.

Mary T LitzingerLaboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Kenneth A Foon
Helen Sabzevari
Kwong-Yok Tsang
Jeffrey Schlom
Claudia Palena
National Institutes of Health · USCenter for Cancer Research · USNational Cancer Institute · USUPMC Hillman Cancer Center · US

Funding

Human T Cell Responses to Tumor Antigens for Cancer Vaccine DevelopmentZIABC010598 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SCHLOM, JEFFREY · 2009 to 2025
$19.3M
Identification of human tumor-associated antigensZIABC010972 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TSANG, KWONG YOK · 2009 to 2016
$6.0M
Human T Cell Responses to Tumor Antigens for Cancer Vaccine DevelopmentZ01BC010598 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SCHLOM, JEFFREY · 2005 to 2008
$2.9M
Intramural NIH HHS Z01 BC010598
6 · The paper itself

Abstract

In chronic lymphocytic leukemia (CLL), malignant B cells and nonmalignant T cells exhibit dysfunction. We previously demonstrated that infection of CLL cells with modified vaccinia Ankara (MVA) expressing the costimulatory molecules B7-1, ICAM-1, and LFA-3 (designated TRICOM) increased expression of these costimulatory molecules on the surface of CLL cells and thus augmented their antigen-presenting capability. Here, we evaluate the effect of MVA-TRICOM-modified CLL cells on T cells. Following incubation with irradiated MVA-TRICOM-modified CLL cells, allogeneic and autologous CD4(+) and CD8(+) T cells expressed significantly higher levels of B7-1, ICAM-1, and LFA-3. We show that this increase was the result of physical acquisition from the antigen-presenting cells (APCs), and that purified T cells that acquired costimulatory molecules from MVA-TRICOM-modified CLL cells were able to stimulate the proliferation of untreated T cells. These results demonstrate for the first time that T cells from CLL patients can acquire multiple costimulatory molecules from autologous CLL cells and can then act as APCs themselves. Given the immunodeficiencies characteristic of CLL, enhancing the antigen-presenting function of CLL cells and T cells simultaneously could be a distinct advantage in the effort to elicit antitumor immune responses.

Indexed as

Antigen-Presenting CellsB7-1 AntigenCD58 AntigensHumansIntercellular Adhesion Molecule-1Leukemia, Lymphocytic, Chronic, B-CellReverse Transcriptase Polymerase Chain ReactionRNA, MessengerT-LymphocytesTumor Cells, CulturedVaccinia virusB7-1 AntigenCD58 AntigensIntercellular Adhesion Molecule-1RNA, Messenger

Identifiers

PMID19009294
PMCPMC2664396
OpenAlexW2059702676

What OpenQuestion holds

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LicenceTDM
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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.