Evidence map›Paper›PMID 31566578›Full record

ArticleThe Journal of clinical investigation2019

β2 adrenergic receptor-mediated signaling regulates the immunosuppressive potential of myeloid-derived suppressor cells.

Hemn Mohammadpour, Cameron R MacDonald, Guanxi Qiao, Minhui Chen, Bowen Dong, Bonnie L Hylander, Philip L McCarthy, Scott I Abrams, Elizabeth A Repasky

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
209citing papers in PubMed, 3 pooled it
15.8field-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

209 citing papers in PubMed, 3 syntheses or guidelines pooled it, 270 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Hemn MohammadpourDepartment of Immunology, and.
Cameron R MacDonaldDepartment of Immunology, and.
Guanxi QiaoDepartment of Immunology, and.
Minhui ChenDepartment of Immunology, and.
Bowen DongDepartment of Immunology, and.
Bonnie L HylanderDepartment of Immunology, and.
Philip L McCarthyDepartment of Medicine, Roswell Park Comprehensive Cancer Center, Buffalo, New York, USA.
Scott I AbramsDepartment of Immunology, and.
Elizabeth A RepaskyDepartment of Immunology, and.
Roswell Park Comprehensive Cancer Center · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
Large heat shock proteins and their role in cancer therapyR01CA099326 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI REPASKY, ELIZABETH A, WANG, XIANG-YANG SHAWN · 2003 to 2020
$5.7M
Understanding how adrenergic signaling influences immune contexture of tumors and the efficacy of checkpoint inhibitorsR01CA205246 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI REPASKY, ELIZABETH A · 2018 to 2022
$2.8M
Mechanisms Underlying Functional Programs of Tumor-Associated MacrophagesR01CA172105 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI ABRAMS, SCOTT I. · 2015 to 2019
$2.0M
Overcoming stress driven suppression of the anti-tumor immune response in cancer - understanding the MDSC piece of the puzzleF32CA239356 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MOHAMMADPOUR, HEMN · 2020 to 2021
$80k
NCI NIH HHS F32 CA239356NCI NIH HHS P30 CA016056NCI NIH HHS R01 CA099326NCI NIH HHS R01 CA172105NCI NIH HHS R01 CA205246
6 · The paper itself

Abstract

Catecholamines released by sympathetic nerves can activate adrenergic receptors present on nearly every cell type, including myeloid-derived suppressor cells (MDSCs). Using in vitro systems, murine tumor models in wild-type and genetically modified (β2-AR-/-) mice, and adoptive transfer approaches, we found that the degree of β2-AR signaling significantly influences MDSC frequency and survival in tumors and other tissues. It also modulates their expression of immunosuppressive molecules such as arginase-I and PD-L1 and alters their ability to suppress the proliferation of T cells. The regulatory functions of β2-AR signaling in MDSCs were also found to be dependent upon STAT3 phosphorylation. Moreover, we observed that the β2-AR-mediated increase in MDSC survival is dependent upon Fas-FasL interactions, and this is consistent with gene expression analyses, which reveal a greater expression of apoptosis-related genes in β2-AR-/- MDSCs. Our data reveal the potential of β2-AR signaling to increase the generation of MDSCs from both murine and human peripheral blood cells and that the immunosuppressive function of MDSCs can be mitigated by treatment with β-AR antagonists, or enhanced by β-AR agonists. This strongly supports the possibility that reducing stress-induced activation of β2-ARs could help to overcome immune suppression and enhance the efficacy of immunotherapy and other cancer therapies.

Indexed as

Immune ToleranceAnimalsMiceMice, Inbred BALB CMice, Inbred C57BLMyeloid-Derived Suppressor CellsNeoplasmsPhosphorylationReceptors, Adrenergic, beta-2Signal TransductionSTAT3 Transcription FactorADRB2 protein, mouseReceptors, Adrenergic, beta-2Stat3 protein, mouseSTAT3 Transcription FactorCancer immunotherapyCellular immune responseG-protein coupled receptorsImmunologyOncology

Identifiers

PMID31566578
PMCPMC6877316
OpenAlexW2978526767

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.