Evidence map›Paper›PMID 39461876›Full record

ArticleJournal for immunotherapy of cancer2024

Dendritic cell-intrinsic PTPN22 negatively regulates antitumor immunity and impacts anti-PD-L1 efficacy.

Santiago Acero-Bedoya, Emily F Higgs, Anna C Martinez, Ruxandra Tonea, Thomas F Gajewski

Abstract 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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Immuno-oncology recapitulates ontogeny: Modern cell and gene therapy for cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    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

5 authors.

Santiago Acero-BedoyaPathology, University of Chicago Biological Sciences Division, Chicago, Illinois, USA.ORCID 0000-0002-2204-7200
Emily F HiggsPathology, Department of Medicine, University of Chicago, Chicago, Illinois, USA.ORCID 0000-0003-2477-8549
Anna C MartinezPathology, University of Chicago Biological Sciences Division, Chicago, Illinois, USA.
Ruxandra ToneaPathology, University of Chicago Biological Sciences Division, Chicago, Illinois, USA.
Thomas F GajewskiPathology and Medicine, The University of Chicago Biological Sciences Division, Chicago, Illinois, USA tgajewsk@medicine.bsd.uchicago.edu.

Funding

Ruth L. Kirschstein National Research Service Award (NRSA) Institutional Research Training Grant (Parent T32)T32HD007009 · NICHD · UNIVERSITY OF CHICAGO · PI NANCY B SCHWARTZ · 1985 to 2026
$13.0M
Overcoming resistance to anti-PD1 immunotherapyR35CA210098 · NCI · UNIVERSITY OF CHICAGO · PI THOMAS F GAJEWSKI · 2017 to 2026
$10.4M
University of Chicago Initiative for Maximizing Student Development (IMSD) - Renewal 01R25GM109439 · NIGMS · UNIVERSITY OF CHICAGO · PI SCHWARTZ, NANCY B · 2014 to 2023
$5.7M
Myeloid cell-expressed PTPN22 and anti-tumor immunityF99CA274689 · NCI · UNIVERSITY OF CHICAGO · PI ACERO BEDOYA, SANTIAGO · 2022 to 2023
$96k
NCI NIH HHS F99 CA274689NCI NIH HHS R35 CA210098NICHD NIH HHS T32 HD007009NIGMS NIH HHS R25 GM109439
6 · The paper itself

Abstract

backgroundIndividuals with a loss-of-function single-nucleotide polymorphism in the gene encoding PTPN22 have an increased risk for autoimmune diseases, and patients with cancer with such alleles may respond better to checkpoint blockade immunotherapy. Studies in PTPN22 knockout (KO) mice have established it as a negative regulator of T cell responses in cancer models. However, the role of PTPN22 in distinct immune cell compartments, such as dendritic cells (DCs), remains undefined.

methodsWe developed a novel PTPN22 conditional KO (cKO) mouse model that enables specific deletion in CD11c

resultsDeletion of PTPN22 in DCs resulted in augmented antitumor immunity in multiple syngeneic tumor models. Tumor antigen-specific CD8

conclusionsDeletion of PTPN22 in DCs is sufficient to drive an augmented tumor antigen-specific T cell response, resulting in enhanced tumor control. PTPN22 negatively regulates DC proliferation and antigen processing and presentation. Our work argues that PTPN22 is an attractive therapeutic target for cancer immunotherapy and highlights the potential to modulate antitumor immunity through the manipulation of DC signaling.

Indexed as

Dendritic CellsProtein Tyrosine Phosphatase, Non-Receptor Type 22AnimalsB7-H1 AntigenHumansImmune Checkpoint InhibitorsImmunotherapyMiceMice, Inbred C57BLMice, KnockoutTumor MicroenvironmentB7-H1 AntigenImmune Checkpoint InhibitorsProtein Tyrosine Phosphatase, Non-Receptor Type 22Ptpn22 protein, mouseDendriticGeneticImmunotherapyMyeloidSolid tumor

Identifiers

PMID39461876
PMCPMC11529514

What OpenQuestion holds

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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.