Evidence map›Paper›PMID 33935280›Full record

ArticleLeukemia2021

Myeloid-derived suppressor cell subtypes differentially influence T-cell function, T-helper subset differentiation, and clinical course in CLL.

Gerardo Ferrer, Byeongho Jung, Pui Yan Chiu, Rukhsana Aslam, Florencia Palacios, Andrea Nicola Mazzarello, Stefano Vergani, Davide Bagnara, Shih-Shih Chen, Sophia Yancopoulos and 10 more

Abstract read
In one paragraph

Article in Leukemia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–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

36 citing papers in PubMed.

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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

20 authors.

Gerardo FerrerKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.ORCID http://orcid.org/0000-0002-4084-6815
Byeongho JungKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Pui Yan ChiuCenter for Immunology & Inflammation, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Rukhsana AslamKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Florencia PalaciosKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Andrea Nicola MazzarelloKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Stefano VerganiKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.ORCID http://orcid.org/0000-0003-0524-5093
Davide BagnaraKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Shih-Shih ChenKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Sophia YancopoulosKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Aliki XochelliInstitute of Applied Biosciences, CERTH, Thessaloniki, Greece.
Xiao-Jie YanKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Jan A BurgerDepartment of Leukemia, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID http://orcid.org/0000-0002-6177-7572
Jacqueline C BarrientosKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Jonathan E KolitzKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Steven L AllenKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.ORCID http://orcid.org/0000-0002-3482-3182
Kostas StamatopoulosInstitute of Applied Biosciences, CERTH, Thessaloniki, Greece.ORCID http://orcid.org/0000-0001-8529-640X
Kanti R RaiKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.ORCID http://orcid.org/0000-0002-5804-2823
Barbara SherryCenter for Immunology & Inflammation, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.ORCID http://orcid.org/0000-0003-3119-1463
Nicholas ChiorazziKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA. NChizzi@Northwell.edu.ORCID http://orcid.org/0000-0003-1023-6650

Funding

Th17 generation, action and therapeutic relevance in chronic lymphocytic leukemiaR01CA238523 · NCI · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI CHIORAZZI, NICHOLAS, SHERRY, BARBARA A · 2020 to 2024
$2.7M
NCI NIH HHS R01 CA238523
6 · The paper itself

Abstract

Cancer pathogenesis involves the interplay of tumor- and microenvironment-derived stimuli. Here we focused on the influence of an immunomodulatory cell type, myeloid-derived suppressor cells (MDSCs), and their lineage-related subtypes on autologous T lymphocytes. Although MDSCs as a group correlated with an immunosuppressive Th repertoire and worse clinical course, MDSC subtypes (polymorphonuclear, PMN-MDSC, and monocytic, M-MDSCs) were often functionally discordant. In vivo, PMN-MDSCs existed in higher numbers, correlated with different Th-subsets, and more strongly associated with poor clinical course than M-MDSCs. In vitro, PMN-MDSCs were more efficient at blocking T-cell growth and promoted Th17 differentiation. Conversely, in vitro M-MDSCs varied in their ability to suppress T-cell proliferation, due to the action of TNFα, and promoted a more immunostimulatory Th compartment. Ibrutinib therapy impacted MDSCs differentially as well, since after initiating therapy, PMN-MDSC numbers progressively declined, whereas M-MDSC numbers were unaffected, leading to a set of less immunosuppressive Th cells. Consistent with this, clinical improvement based on decreasing CLL-cell numbers correlated with the decrease in PMN-MDSCs. Collectively, the data support a balance between PMN-MDSC and M-MDSC numbers and function influencing CLL disease course.

Indexed as

Tumor MicroenvironmentCase-Control StudiesCell DifferentiationCell ProliferationFemaleHumansLeukemia, Lymphocytic, Chronic, B-CellLymphocyte ActivationMaleMonocytesMyeloid-Derived Suppressor CellsTh1 CellsTh2 CellsT-Lymphocytes

Identifiers

PMID33935280
PMCPMC8550941

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.