Evidence map›Paper›PMID 26578623›Full record

ArticleNeuro-oncology2016

CD4+ T effector memory cell dysfunction is associated with the accumulation of granulocytic myeloid-derived suppressor cells in glioblastoma patients.

Daniel Dubinski, Johannes Wölfer, Martin Hasselblatt, Tilman Schneider-Hohendorf, Ulrich Bogdahn, Walter Stummer, Heinz Wiendl, Oliver M Grauer

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuro-oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

130 citing papers in PubMed, 1 synthesis or guideline pooled it.

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70 more citing papers are in PubMed but not listed here.

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

8 authors.

Daniel DubinskiDepartment of Neurology, University Hospital of Regensburg, Regensburg, Germany (D.D., U.B.); Department of Neurosurgery, University Hospital of Muenster, Muenster, Germany (J.W., W.S.); Institute of Neuropathology, University Hospital of Muenster, Muenster, Germany (M.H.); Department of Neurology, University Hospital of Muenster, Muenster, Germany (T.S.-H., H.W., O.M.G.).
Johannes WölferDepartment of Neurology, University Hospital of Regensburg, Regensburg, Germany (D.D., U.B.); Department of Neurosurgery, University Hospital of Muenster, Muenster, Germany (J.W., W.S.); Institute of Neuropathology, University Hospital of Muenster, Muenster, Germany (M.H.); Department of Neurology, University Hospital of Muenster, Muenster, Germany (T.S.-H., H.W., O.M.G.).
Martin HasselblattDepartment of Neurology, University Hospital of Regensburg, Regensburg, Germany (D.D., U.B.); Department of Neurosurgery, University Hospital of Muenster, Muenster, Germany (J.W., W.S.); Institute of Neuropathology, University Hospital of Muenster, Muenster, Germany (M.H.); Department of Neurology, University Hospital of Muenster, Muenster, Germany (T.S.-H., H.W., O.M.G.).
Tilman Schneider-HohendorfDepartment of Neurology, University Hospital of Regensburg, Regensburg, Germany (D.D., U.B.); Department of Neurosurgery, University Hospital of Muenster, Muenster, Germany (J.W., W.S.); Institute of Neuropathology, University Hospital of Muenster, Muenster, Germany (M.H.); Department of Neurology, University Hospital of Muenster, Muenster, Germany (T.S.-H., H.W., O.M.G.).
Ulrich BogdahnDepartment of Neurology, University Hospital of Regensburg, Regensburg, Germany (D.D., U.B.); Department of Neurosurgery, University Hospital of Muenster, Muenster, Germany (J.W., W.S.); Institute of Neuropathology, University Hospital of Muenster, Muenster, Germany (M.H.); Department of Neurology, University Hospital of Muenster, Muenster, Germany (T.S.-H., H.W., O.M.G.).
Walter StummerDepartment of Neurology, University Hospital of Regensburg, Regensburg, Germany (D.D., U.B.); Department of Neurosurgery, University Hospital of Muenster, Muenster, Germany (J.W., W.S.); Institute of Neuropathology, University Hospital of Muenster, Muenster, Germany (M.H.); Department of Neurology, University Hospital of Muenster, Muenster, Germany (T.S.-H., H.W., O.M.G.).
Heinz WiendlDepartment of Neurology, University Hospital of Regensburg, Regensburg, Germany (D.D., U.B.); Department of Neurosurgery, University Hospital of Muenster, Muenster, Germany (J.W., W.S.); Institute of Neuropathology, University Hospital of Muenster, Muenster, Germany (M.H.); Department of Neurology, University Hospital of Muenster, Muenster, Germany (T.S.-H., H.W., O.M.G.).
Oliver M GrauerDepartment of Neurology, University Hospital of Regensburg, Regensburg, Germany (D.D., U.B.); Department of Neurosurgery, University Hospital of Muenster, Muenster, Germany (J.W., W.S.); Institute of Neuropathology, University Hospital of Muenster, Muenster, Germany (M.H.); Department of Neurology, University Hospital of Muenster, Muenster, Germany (T.S.-H., H.W., O.M.G.).

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyeloid-derived suppressor cells (MDSCs) comprise a heterogeneous population of myeloid cells that are significantly expanded in cancer patients and are associated with tumor progression.

methodsMulticolor flow cytometry was used to study the frequency, phenotype, and function of MDSCs in peripheral blood and freshly resected tumors of 52 participants with primary glioblastoma (GBM).

resultsThe frequency of CD14(high)CD15(pos) monocytic and CD14(low)CD15(pos) granulocytic MDSCs was significantly higher in peripheral blood of GBM participants compared with healthy donors. The majority of granulocytic MDSCs consisted of CD14(low)CD15(high) neutrophilic MDSCs with high T-cell suppressive capacities. At the tumor side, we found an increase in CD14(high)CD15(pos) monocytic MDSCs and high frequencies of CD14(low)CD15(pos) granulocytic MDSCs that displayed an activated phenotype with downregulation of CD16 and upregulation of HLA-DR molecules, which did not inhibit T-cell proliferative responses in vitro. However, a strong association between granulocytic MDSCs and CD4(+) effector memory T-cells (TEM) within the tumors was detected. Tumor-derived CD4(+) TEM expressed high levels of PD-1 when compared with their blood-derived counterparts and were functionally exhausted. The respective ligand, PD-L1, was significantly upregulated on tumor-derived MDSCs, and T-cell co-culture experiments confirmed that glioma-infiltrating MDSCs can induce PD-1 expression on CD4(+) TEM.

conclusionsOur findings provide a detailed characterization of different MDSC subsets in GBM patients and indicate that both granulocytic MDSCs in peripheral blood and at the tumor site play a major role in GBM-induced T-cell suppression.

Indexed as

CD4-Positive T-LymphocytesCell ProliferationCoculture TechniquesFlow CytometryGlioblastomaHumansImmunologic MemoryLymphocyte ActivationMonocytesMyeloid CellsMyeloid-Derived Suppressor Cellsglioblastomamyeloid-derived suppressor cellPD-1PD-L1T effector memory cell

Identifiers

PMID26578623
PMCPMC4864257

What OpenQuestion holds

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Registered trials

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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.