Evidence map›Paper›PMID 24446520›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

TNF-α-dependent hematopoiesis following Bcl11b deletion in T cells restricts metastatic melanoma.

Mohammad N Uddin, Yubin Zhang, Jonathan A Harton, Katherine C MacNamara, Dorina Avram

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 16 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Mohammad N UddinCenter for Immunology and Microbial Disease, Albany Medical College, Albany, NY 12208.
Yubin Zhang
Jonathan A Harton
Katherine C MacNamara
Dorina Avram
Albany Medical Center Hospital · US

Funding

Role of Bcl11b in CD4+ T cells and innate lymphoid cellsR01AI067846 · NIAID · UNIVERSITY OF FLORIDA · PI AVRAM, DORINA · 2007 to 2023
$6.2M
Regulation of CD4 T cell Development and Function by BCL11B Transcription FactorR01AI078273 · NIAID · ALBANY MEDICAL COLLEGE · PI AVRAM, DORINA · 2008 to 2012
$1.2M
BCL11B in Immune RegulationR56AI078273 · NIAID · ALBANY MEDICAL COLLEGE · PI AVRAM, DORINA · 2013 to 2013
$205k
NIAID NIH HHS AI067846NIAID NIH HHS AI078273NIAID NIH HHS R01 AI067846NIAID NIH HHS R01 AI078273NIAID NIH HHS R56 AI078273
6 · The paper itself

Abstract

Using several tumor models, we demonstrate that mice deficient in Bcl11b in T cells, although having reduced numbers of T cells in the peripheral lymphoid organs, developed significantly less tumors compared with wild-type mice. Bcl11b(-/-) CD4(+) T cells, with elevated TNF-α levels, but not the Bcl11b(-/-) CD8(+) T cells, were required for the reduced tumor burden, as were NK1.1(+) cells, found in increased numbers in Bcl11b(F/F)/CD4-Cre mice. Among NK1.1(+) cells, the NK cell population was predominant in number and was the only population displaying elevated granzyme B levels and increased degranulation, although not increased proliferation. Although the number of myeloid-derived suppressor cells was increased in the lungs with metastatic tumors of Bcl11b(F/F)/CD4-Cre mice, their arginase-1 levels were severely reduced. The increase in NK cell and myeloid-derived suppressor cell numbers was associated with increased bone marrow and splenic hematopoiesis. Finally, the reduced tumor burden, increased numbers of NK cells in the lung, and increased hematopoiesis in Bcl11b(F/F)/CD4-Cre mice were all dependent on TNF-α. Moreover, TNF-α treatment of wild-type mice also reduced the tumor burden and increased hematopoiesis and the numbers and activity of NK cells in the lung. In vitro treatment with TNF-α of lineage-negative hematopoietic progenitors increased NK and myeloid differentiation, further supporting a role of TNF-α in promoting hematopoiesis. These studies reveal a novel role for TNF-α in the antitumor immune response, specifically in stimulating hematopoiesis and increasing the numbers and activity of NK cells.

Indexed as

AnimalsAntigens, LyArginaseCD8-Positive T-LymphocytesCell DegranulationCell ProliferationGene DeletionGranzymesHematopoiesisKiller Cells, NaturalLung NeoplasmsLymphocyte CountMelanomaMiceMice, TransgenicMyeloid CellsAntigens, LyArg1 protein, mouseArginaseBcl11b protein, mouseGranzymesKlrb1c protein, mouseNK Cell Lectin-Like Receptor Subfamily BRepressor ProteinsTumor Necrosis Factor-alphaTumor Suppressor Proteins

Identifiers

PMID24446520
PMCPMC3946214
OpenAlexW2112855928

What OpenQuestion holds

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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.