Evidence map›Paper›PMID 24938765›Full record

ArticleCancer research2014

Engineered fusokine GIFT4 licenses the ability of B cells to trigger a tumoricidal T-cell response.

Jiusheng Deng, Shala Yuan, Andrea Pennati, Jordan Murphy, Jian Hui Wu, David Lawson, Jacques Galipeau

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 28 citations in OpenAlex.

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  10. Article
  11. Regulatory B cells in cancer.Immunological reviews · 2021
    Review
  12. Review
  13. Review
  14. GM-CSF and IL-4 Fusion Cytokine Induces B Cell-Dependent Hematopoietic Regeneration.Molecular therapy : the journal of the American Society of Gene Therapy · 2017
    Article
  15. Article
  16. Article
  17. Review
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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

7 authors at 2 institutions in 2 countries.

Jiusheng DengDepartment of Hematology and Medical Oncology, Winship Cancer Institute, Emory University, Atlanta, Georgia.
Shala YuanDepartment of Hematology and Medical Oncology, Winship Cancer Institute, Emory University, Atlanta, Georgia.
Andrea PennatiDepartment of Hematology and Medical Oncology, Winship Cancer Institute, Emory University, Atlanta, Georgia.
Jordan MurphyDepartment of Hematology and Medical Oncology, Winship Cancer Institute, Emory University, Atlanta, Georgia.
Jian Hui WuLady Davis Institute for Medical Research, Department of Oncology, McGill University, Quebec, Canada.
David LawsonDepartment of Hematology and Medical Oncology, Winship Cancer Institute, Emory University, Atlanta, Georgia.
Jacques GalipeauDepartment of Hematology and Medical Oncology, Winship Cancer Institute, Emory University, Atlanta, Georgia. jgalipe@emory.edu.
Emory University · USMcGill University · CA

Funding

Winship Cancer Institute Cancer Center Support GrantP30CA138292 · NCI · EMORY UNIVERSITY · PI Suresh S Ramalingam · 2009 to 2026
$47.5M
Inducible B-regulatory cells (iBREGs) for treatment of Multiple SclerosisR01AI093881 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI GALIPEAU, JACQUES · 2012 to 2016
$1.9M
NCI NIH HHS P30 CA138292NIAID NIH HHS 5R01AI093881NIAID NIH HHS R01 AI093881
6 · The paper itself

Abstract

Engineered chimeric cytokines can generate gain-of-function activity in immune cells. Here, we report potent antitumor activity for a novel fusion cytokine generated by N-terminal coupling of GM-CSF to IL4, generating a fusokine termed GIFT4. B cells treated with GIFT4 clustered GM-CSF and IL4 receptors on the cell surface and displayed a pan-STAT hyperphosphorylation associated with acquisition of a distinct phenotype and function described to date. In C57BL/6J mice, administration of GIFT4 expanded endogenous B cells and suppressed the growth of B16F0 melanoma cells. Furthermore, B16F0 melanoma cells engineered to secrete GIFT4 were rejected immunologically in a B-cell-dependent manner. This effect was abolished when GIFT4-expressing B16F0 cells were implanted in B-cell-deficient mice, confirming a B-cell-dependent antitumor effect. Human GIFT4-licensed B cells primed cytotoxic T cells and specifically killed melanoma cells in vitro and in vivo. Taken together, our results demonstrated that GIFT4 could mediate expansion of B cells with potent antigen-specific effector function. GIFT4 may offer a novel immunotherapeutic tool and define a previously unrecognized potential for B cells in melanoma immunotherapy.

Indexed as

AnimalsB-LymphocytesCell Growth ProcessesGenetic EngineeringGranulocyte-Macrophage Colony-Stimulating FactorHumansInterleukin-4Melanoma, ExperimentalMiceMice, Inbred C57BLMicroscopy, ConfocalProtein EngineeringRecombinant Fusion ProteinsT-Lymphocytes, CytotoxicGranulocyte-Macrophage Colony-Stimulating FactorIL4 protein, humanInterleukin-4Recombinant Fusion Proteins

Identifiers

PMID24938765
PMCPMC4119532
OpenAlexW2161246322

What OpenQuestion holds

Textmetadata
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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.