Evidence map›Paper›PMID 21734236›Full record

ArticleBlood2011

A human promyelocytic-like population is responsible for the immune suppression mediated by myeloid-derived suppressor cells.

Samantha Solito, Erika Falisi, Claudia Marcela Diaz-Montero, Andrea Doni, Laura Pinton, Antonio Rosato, Samuela Francescato, Giuseppe Basso, Paola Zanovello, Georgiana Onicescu and 4 more

Open access · greenAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
203citing papers in PubMed, 3 pooled it
12.8field-weighted citation impact, top 1% 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

203 citing papers in PubMed, 3 syntheses or guidelines pooled it, 330 citations in OpenAlex.

  1. Hyperprogressive disease in carcinoma induced by immune checkpoint inhibitor therapy: a systematic review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  20. Mechanisms of Anti-PD Therapy Resistance in Digestive System Neoplasms.Recent patents on anti-cancer drug discovery · 2025
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143 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

14 authors at 6 institutions in 2 countries.

Samantha SolitoDepartment of Oncology and Surgical Sciences, Oncology Section, University of Padova, Padova, Italy.
Erika Falisi
Claudia Marcela Diaz-Montero
Andrea Doni
Laura Pinton
Antonio Rosato
Samuela Francescato
Giuseppe Basso
Paola Zanovello
Georgiana Onicescu
Elizabeth Garrett-Mayer
Alberto J Montero
Vincenzo Bronte
Susanna Mandruzzato
University of Padua · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITMedical University of South Carolina · USIstituto Oncologico Veneto · ITSylvester Comprehensive Cancer Center · USUniversity of Miami · US

Funding

Enhancing T-Cell Responses with the Glutathione Mimetic NOV-002 in Breast CancerK23CA148893 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MONTERO, ALBERTO JOSE · 2010 to 2014
$798k
Programming T Cells for Successful Adoptive Cell TherapyK01CA134927 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI DIAZ-MONTERO, CLAUDIA MARCELA · 2009 to 2013
$645k
NCI NIH HHS K01 CA134927NCI NIH HHS K23 CA148893
6 · The paper itself

Abstract

We recently demonstrated that human BM cells can be treated in vitro with defined growth factors to induce the rapid generation of myeloid-derived suppressor cells (MDSCs), hereafter defined as BM-MDSCs. Indeed, combination of G-CSF + GM-CSF led to the development of a heterogeneous mixture of immature myeloid cells ranging from myeloblasts to band cells that were able to suppress alloantigen- and mitogen-stimulated T lymphocytes. Here, we further investigate the mechanism of suppression and define the cell subset that is fully responsible for BM-MDSC-mediated immune suppression. This population, which displays the structure and markers of promyelocytes, is however distinct from physiologic promyelocytes that, instead, are devoid of immuosuppressive function. In addition, we demonstrate that promyelocyte-like cells proliferate in the presence of activated lymphocytes and that, when these cells exert suppressive activity, they do not differentiate but rather maintain their immature phenotype. Finally, we show that promyelocyte-like BM-MDSCs are equivalent to MDSCs present in the blood of patients with breast cancer and patients with colorectal cancer and that increased circulating levels of these immunosuppressive myeloid cells correlate with worse prognosis and radiographic progression.

Indexed as

Immune ToleranceBreast NeoplasmsCD11b AntigenCD3 ComplexCD8-Positive T-LymphocytesCell DifferentiationCell ProliferationColorectal NeoplasmsFemaleGPI-Linked ProteinsHumansIn Vitro TechniquesLeukemia, LymphoidLymphocyte ActivationMaleMyeloid CellsCD11b AntigenCD3 antigen, zeta chainCD3 ComplexFCGR3B protein, humanGPI-Linked ProteinsITGAM protein, humanReceptors, IgG

Identifiers

PMID21734236
PMCPMC3709641
OpenAlexW2078132657

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.