Evidence map›Paper›PMID 30181177›Full record

ReviewCancer research2018

Treg Destabilization and Reprogramming: Implications for Cancer Immunotherapy.

David H Munn, Madhav D Sharma, Theodore S Johnson

Open access · greenAbstract readReview
In one paragraph

Review in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

60 citing papers in PubMed, 83 citations in OpenAlex.

  1. Trial
  2. Regulatory T cells in cancer and inflammation.Signal transduction and targeted therapy · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Immunosuppressive JAG2Cancer communications (London, England) · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Manipulating the EphB4-ephrinB2 axis to reduce metastasis in HNSCC.bioRxiv : the preprint server for biology · 2024
    Article
  16. Article
  17. Review
  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

3 authors at 1 institution in 2 countries.

David H MunnGeorgia Cancer Center, Augusta University, Augusta, Georgia. dmunn@augusta.edu.
Madhav D SharmaGeorgia Cancer Center, Augusta University, Augusta, Georgia.
Theodore S JohnsonGeorgia Cancer Center, Augusta University, Augusta, Georgia.
Augusta University · US

Funding

Reprogramming the TME for immunogenic antigen-presentationR01CA103320 · NCI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI MUNN, DAVID H. · 2003 to 2024
$6.0M
PTEN, Tregs and MDSCs in the tumor microenvironmentR01CA211229 · NCI · AUGUSTA UNIVERSITY · PI MUNN, DAVID H. · 2017 to 2021
$1.7M
P53-dependent immunogenic DCs in the tumor microenvironmentR50CA232983 · NCI · AUGUSTA UNIVERSITY · PI SHARMA, MADHAV DATT · 2018 to 2020
$614k
NCI NIH HHS R01 CA103320NCI NIH HHS R01 CA211229NCI NIH HHS R50 CA232983
6 · The paper itself

Abstract

Regulatory T cells (Tregs) are an important contributor to the immunosuppressive tumor microenvironment. To date, however, they have been difficult to target for therapy. One emerging new aspect of Treg biology is their apparent functional instability in the face of certain acute proinflammatory signals such as IL6 and IFNγ. Under the right conditions, these signals can cause a rapid loss of suppressor activity and reprogramming of the Tregs into a proinflammatory phenotype. In this review, we propose the hypothesis that this phenotypic modulation does not reflect infidelity to the Treg lineage, but rather represents a natural, physiologic response of Tregs during beneficial inflammation. In tumors, however, this inflammation-induced Treg destabilization is actively opposed by dominant stabilizing factors such as indoleamine 2,3-dioxygenase and the PTEN phosphatase pathway in Tregs. Under such conditions, tumor-associated Tregs remain highly suppressive and inhibit cross-presentation of tumor antigens released by dying tumor cells. Interrupting these Treg stabilizing pathways can render tumor-associated Tregs sensitive to rapid destabilization during immunotherapy, or during the wave of cell death following chemotherapy or radiation, thus enhancing antitumor immune responses. Understanding the emerging pathways of Treg stabilization and destabilization may reveal new molecular targets for therapy.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCell LineageCell Line, TumorDown-RegulationHumansImmune SystemImmunotherapyInflammationInterferon-gammaInterleukin-6NeoplasmsPhenotypePTEN PhosphohydrolaseReceptors, Antigen, T-CellT-Lymphocytes, RegulatoryIL6 protein, humanInterferon-gammaInterleukin-6PTEN PhosphohydrolaseReceptors, Antigen, T-Cell

Identifiers

PMID30181177
PMCPMC6139039
OpenAlexW2890334478

What OpenQuestion holds

Textmetadata
LicenceTDM
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.