Evidence map›Paper›PMID 38580330›Full record

ArticleJournal for immunotherapy of cancer2024

Pyroptosis activates conventional type I dendritic cells to mediate the priming of highly functional anticancer T cells.

Jordon M Inkol, Michael J Westerveld, Shayla G Verburg, Scott R Walsh, Jodi Morrison, Karen L Mossman, Sarah M Worfolk, Kaslyn Lf Kallio, Noah J Phippen, Rebecca Burchett and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Pyroptosis: Turning Up the Heat on Cancer.Annual review of immunology · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
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

13 authors at 2 institutions in 1 country.

Jordon M InkolDepartment of Pathobiology, University of Guelph, Guelph, Ontario, Canada.
Michael J WesterveldDepartment of Pathobiology, University of Guelph, Guelph, Ontario, Canada.
Shayla G VerburgDepartment of Pathobiology, University of Guelph, Guelph, Ontario, Canada.
Scott R WalshDepartment of Pathobiology, University of Guelph, Guelph, Ontario, Canada.
Jodi MorrisonDepartment of Biomedical Sciences, University of Guelph, Guelph, Ontario, Canada.
Karen L MossmanDepartment of Medicine, McMaster University, Hamilton, Ontario, Canada.
Sarah M WorfolkDepartment of Pathobiology, University of Guelph, Guelph, Ontario, Canada.
Kaslyn Lf KallioDepartment of Pathobiology, University of Guelph, Guelph, Ontario, Canada.
Noah J PhippenDepartment of Pathobiology, University of Guelph, Guelph, Ontario, Canada.
Rebecca BurchettPathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada.
Yonghong WanPathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada.
Jonathan BramsonPathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada.ORCID 0000-0003-2874-6886
Samuel T WorkenheDepartment of Pathobiology, University of Guelph, Guelph, Ontario, Canada sworkenh@uoguelph.ca.ORCID 0000-0001-9521-3903
University of Guelph · CAMcMaster University · CA

Funding

CIHR
6 · The paper itself

Abstract

backgroundInitiation of antitumor immunity is reliant on the stimulation of dendritic cells (DCs) to present tumor antigens to naïve T cells and generate effector T cells that can kill cancer cells. Induction of immunogenic cell death after certain types of cytotoxic anticancer therapies can stimulate T cell-mediated immunity. However, cytotoxic therapies simultaneously activate multiple types of cellular stress and programmed cell death; hence, it remains unknown what types of cancer cell death confer superior antitumor immunity.

methodsMurine cancer cells were engineered to activate apoptotic or pyroptotic cell death after Dox-induced expression of procell death proteins. Cell-free supernatants were collected to measure secreted danger signals, cytokines, and chemokines. Tumors were formed by transplanting engineered tumor cells to specifically activate apoptosis or pyroptosis in established tumors and the magnitude of immune response measured by flow cytometry. Tumor growth was measured using calipers to estimate end point tumor volumes for Kaplan-Meier survival analysis.

resultsWe demonstrated that, unlike apoptosis, pyroptosis induces an immunostimulatory secretome signature. In established tumors pyroptosis preferentially activated CD103

conclusionOur study highlights that distinct types of cell death yield varying immunotherapeutic effect and selective activation of pyroptosis can be used to potentiate multiple aspects of the anticancer immunity cycle.

Indexed as

CD8-Positive T-LymphocytesNeoplasmsAnimalsCytokinesDendritic CellsMicePyroptosisCytokinesAdaptive ImmunityAdjuvants, ImmunologicAntigen PresentationBiomarkers, TumorImmunity

Identifiers

PMID38580330
PMCPMC11002387
OpenAlexW4393989214

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.