Evidence map›Paper›PMID 34228641›Full record

ArticleThe Journal of clinical investigation2021

Distinct mechanisms govern populations of myeloid-derived suppressor cells in chronic viral infection and cancer.

Evgenii N Tcyganov, Shino Hanabuchi, Ayumi Hashimoto, David Campbell, Gozde Kar, Timothy Wf Slidel, Corinne Cayatte, Aimee Landry, Fernanda Pilataxi, Susana Hayes and 12 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing 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

54 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. IL1RAJournal of clinical and translational hepatology · 2025
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

22 authors.

Evgenii N TcyganovImmunology, Microenvironment, and Metastasis Program, The Wistar Institute, Philadelphia, Pennsylvania, USA.
Shino HanabuchiAstraZeneca, Gaithersburg, Maryland, USA.
Ayumi HashimotoImmunology, Microenvironment, and Metastasis Program, The Wistar Institute, Philadelphia, Pennsylvania, USA.
David CampbellAstraZeneca, Gaithersburg, Maryland, USA.
Gozde KarAstraZeneca, Translational Medicine, Research and Early Development, Oncology Research & Development, Cambridge, United Kingdom.
Timothy Wf SlidelAstraZeneca, Translational Medicine, Research and Early Development, Oncology Research & Development, Cambridge, United Kingdom.
Corinne CayatteAstraZeneca, Gaithersburg, Maryland, USA.
Aimee LandryAstraZeneca, Gaithersburg, Maryland, USA.
Fernanda PilataxiAstraZeneca, Gaithersburg, Maryland, USA.
Susana HayesAstraZeneca, Gaithersburg, Maryland, USA.
Brian DoughertyAstraZeneca, Gaithersburg, Maryland, USA.
Kristin C HicksAstraZeneca, Gaithersburg, Maryland, USA.
Kathy MulgrewAstraZeneca, Gaithersburg, Maryland, USA.
Chih-Hang Anthony TangImmunology, Microenvironment, and Metastasis Program, The Wistar Institute, Philadelphia, Pennsylvania, USA.
Chih-Chi Andrew HuImmunology, Microenvironment, and Metastasis Program, The Wistar Institute, Philadelphia, Pennsylvania, USA.
Wei GuoCancer Prevention and Control Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania, USA.
Sergei GrivennikovCancer Prevention and Control Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania, USA.
Mohammed-Alkhatim A AliDepartment of Systems Pharmacology and Translational Therapeutics and.
Jean-Christophe BeltraDepartment of Systems Pharmacology and Translational Therapeutics and.
E John WherryDepartment of Systems Pharmacology and Translational Therapeutics and.
Yulia NefedovaImmunology, Microenvironment, and Metastasis Program, The Wistar Institute, Philadelphia, Pennsylvania, USA.
Dmitry I GabrilovichAstraZeneca, Gaithersburg, Maryland, USA.

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
Targeting ER stress response in B-cell chronic lymphocytic leukemiaR01CA163910 · NCI · WISTAR INSTITUTE · PI Chih-Chi Andrew Hu · 2013 to 2026
$4.8M
Mechanism of myeloid cell defect in cancerR01CA100062 · NCI · WISTAR INSTITUTE · PI GABRILOVICH, DMITRY I · 2004 to 2018
$4.0M
Negative regulation of myeloid-derived suppressive cells in cancerR01CA216936 · NCI · WISTAR INSTITUTE · PI FUCHS, SERGE Y, NEFEDOVA, YULIA · 2018 to 2022
$2.5M
The role of Interleukin 17RB signaling in colorectal cancer progressionR01CA227629 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI GRIVENNIKOV, SERGEI I · 2018 to 2022
$2.5M
Mechanisms of cytokine driven tumor elicited inflammation in colorectal cancerR01CA218133 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI GRIVENNIKOV, SERGEI I · 2018 to 2022
$2.4M
NCI NIH HHS P30 CA010815NCI NIH HHS R01 CA100062NCI NIH HHS R01 CA163910NCI NIH HHS R01 CA216936NCI NIH HHS R01 CA218133NCI NIH HHS R01 CA227629
6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) are major negative regulators of immune responses in cancer and chronic infections. It remains unclear if regulation of MDSC activity in different conditions is controlled by similar mechanisms. We compared MDSCs in mice with cancer and lymphocytic choriomeningitis virus (LCMV) infection. Chronic LCMV infection caused the development of monocytic MDSCs (M-MDSCs) but did not induce polymorphonuclear MDSCs (PMN-MDSCs). In contrast, both MDSC populations were present in cancer models. An acquisition of immune-suppressive activity by PMN-MDSCs in cancer was controlled by IRE1α and ATF6 pathways of the endoplasmic reticulum (ER) stress response. Abrogation of PMN-MDSC activity by blockade of the ER stress response resulted in an increase in tumor-specific immune response and reduced tumor progression. In contrast, the ER stress response was dispensable for suppressive activity of M-MDSCs in cancer and LCMV infection. Acquisition of immune-suppressive activity by M-MDSCs in spleens was mediated by IFN-γ signaling. However, it was dispensable for suppressive activity of M-MDSCs in tumor tissues. Suppressive activity of M-MDSCs in tumors was retained due to the effect of IL-6 present at high concentrations in the tumor site. These results demonstrate disease- and population-specific mechanisms of MDSC accumulation and the need for targeting different pathways to achieve inactivation of these cells.

Indexed as

AnimalsCell Line, TumorChronic DiseaseEndoplasmic Reticulum StressFemaleHumansImmune ToleranceInterferon-gammaLymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMaleMiceMice, Inbred C57BLMice, KnockoutMyeloid-Derived Suppressor CellsNeoplasmsIFNG protein, mouseInterferon-gammaImmunologyInnate immunityMonocytesNeutrophilsOncology

Identifiers

PMID34228641
PMCPMC8363287

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.