Evidence map›Paper›PMID 25085111›Full record

ArticleJournal of leukocyte biology2014

Liver metastases induce reversible hepatic B cell dysfunction mediated by Gr-1+CD11b+ myeloid cells.

Mitchell Thorn, Gary R Point, Rachel A Burga, Cang T Nguyen, N Joseph Espat, Steven C Katz

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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  13. Hepatic myeloid-derived suppressor cells in cancer.Cancer immunology, immunotherapy : CII · 2015
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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

6 authors at 3 institutions in 1 country.

Mitchell ThornRoger Williams Medical Center, Department of Surgery, Providence, Rhode Island, USA; and Boston University School of Medicine, Boston, Massachusetts, USA mitchell.thorn@chartercare.org.
Gary R PointRoger Williams Medical Center, Department of Surgery, Providence, Rhode Island, USA; and.
Rachel A BurgaRoger Williams Medical Center, Department of Surgery, Providence, Rhode Island, USA; and.
Cang T NguyenRoger Williams Medical Center, Department of Surgery, Providence, Rhode Island, USA; and.
N Joseph EspatRoger Williams Medical Center, Department of Surgery, Providence, Rhode Island, USA; and Boston University School of Medicine, Boston, Massachusetts, USA.
Steven C KatzRoger Williams Medical Center, Department of Surgery, Providence, Rhode Island, USA; and Boston University School of Medicine, Boston, Massachusetts, USA.
Roger Williams Medical Center · USProvidence College · USBoston University · US

Funding

Reversing genetically modified T cell suppression in a model of liver metastasesK08CA160662 · NCI · ROGER WILLIAMS MEDICAL CENTER · PI KATZ, STEVEN C · 2012 to 2016
$838k
NCI NIH HHS 1K08CA160662-01A1NCI NIH HHS K08 CA160662
6 · The paper itself

Abstract

LM escape immune surveillance, in part, as a result of the expansion of CD11b+MC, which alter the intrahepatic microenvironment to promote tumor tolerance. HBC make up a significant proportion of liver lymphocytes and appear to delay tumor progression; however, their significance in the setting of LM is poorly defined. Therefore, we characterized HBC and HBC/CD11b+MC interactions using a murine model of LM. Tumor-bearing livers showed a trend toward elevated absolute numbers of CD19+ HBC. A significant increase in the frequency of IgM(lo)IgD(hi) mature HBC was observed in mice with LM compared with normal mice. HBC derived from tumor-bearing mice demonstrated increased proliferation in response to TLR and BCR stimulation ex vivo compared with HBC from normal livers. HBC from tumor-bearing livers exhibited significant down-regulation of CD80 and were impaired in inducing CD4(+) T cell proliferation ex vivo. We implicated hepatic CD11b+MC as mediators of CD80 down-modulation on HBC ex vivo via a CD11b-dependent mechanism that required cell-to-cell contact and STAT3 activity. Therefore, CD11b+MC may compromise the ability of HBC to promote T cell activation in the setting of LM as a result of diminished expression of CD80. Cross-talk between CD11b+MC and HBC may be an important component of LM-induced immunosuppression.

Indexed as

Adoptive TransferAnimalsB7-1 AntigenB7-2 AntigenB-Lymphocyte SubsetsCD11b AntigenCell Line, TumorDisease Models, AnimalDown-RegulationLiver NeoplasmsLuminescent MeasurementsLymphocyte ActivationMaleMiceMolecular ImagingMyeloid CellsB7-1 AntigenB7-2 AntigenCD11b Antigengranulocyte receptor 1, mouseReceptors, Cell SurfaceB cellsimmunosuppressionliverSTAT3

Identifiers

PMID25085111
PMCPMC4197561
OpenAlexW2110849049

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.