Evidence map›Paper›PMID 34858727›Full record

ArticleOncoimmunology2021

Tumor cell-derived IL-10 promotes cell-autonomous growth and immune escape in diffuse large B-cell lymphoma.

Kristin Stirm, Peter Leary, Katrin Bertram, Nicolás Gonzalo Núñez, Daria Wüst, Christophe Boudesco, Els Verhoeyen, Thorsten Zenz, Burkhard Becher, Thomas Menter and 2 more

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 43 citations in OpenAlex.

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  14. TRAF3 loss-of-function reveals the noncanonical NF-κB pathway as a therapeutic target in diffuse large B cell lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

12 authors at 3 institutions in 4 countries.

Kristin StirmInstitute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.
Peter LearyInstitute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.
Katrin BertramInstitute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.
Nicolás Gonzalo NúñezInstitute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
Daria WüstInstitute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.
Christophe BoudescoInstitute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.
Els VerhoeyenCIRI, Université de Lyon; Inserm U1111; Ens de Lyon, France.
Thorsten ZenzDepartment of Medical Oncology and Hematology, University Hospital Zurich and University of Zurich, Zurich, Switzerland.
Burkhard BecherInstitute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
Thomas MenterInstitute of Medical Genetics and Pathology, University Hospital Basel, University of Basel, Switzerland.ORCID 0000-0002-0847-6156
Alexandar TzankovInstitute of Medical Genetics and Pathology, University Hospital Basel, University of Basel, Switzerland.
Anne MüllerInstitute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.
University of Zurich · CHUniversity of Basel · CHUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diffuse large B-cell lymphoma (DLBCL) is an aggressive malignancy arising from germinal center or post-germinal center B-cells that retain many of the properties of normal B-cells. Here we show that a subset of DLBCL express the cytokine IL-10 and its receptor. The genetic ablation of IL-10 receptor signaling abrogates the autocrine STAT3 phosphorylation triggered by tumor cell-intrinsic IL-10 expression and impairs growth of DLBCL cell lines in subcutaneous and orthotopic xenotransplantation models. Furthermore, we demonstrate using an immunocompetent Myc-driven model of DLBCL that neutralization of IL-10 signaling reduces tumor growth, which can be attributed to reduced Treg infiltration, stronger intratumoral effector T-cell responses, and restored tumor-specific MHCII expression. The effects of IL-10R neutralization were phenocopied by the genetic ablation of IL-10 signaling in the Treg compartment and could be reversed by MHCII blockade. The BTK inhibitor ibrutinib effectively blocked tumor cell-intrinsic IL-10 expression and tumor growth in this Myc-driven model. Tumors from patients with high IL-10RA expression are infiltrated by higher numbers of Tregs than IL-10RA

Indexed as

Interleukin-10Lymphoma, Large B-Cell, DiffuseCell Line, TumorCell ProliferationGerminal CenterHumansIL10 protein, humanInterleukin-10cancer immunotherapyDLBCL mouse modelsLymphoma microenvironmentoncogenic STAT3 signalingpersonalized treatment

Identifiers

PMID34858727
PMCPMC8632300
OpenAlexW3215525273

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.