Evidence map›Paper›PMID 36099917›Full record

ArticleCell reports. Medicine2022

Balance between immunoregulatory B cells and plasma cells drives pancreatic tumor immunity.

Bhalchandra Mirlekar, Yan Wang, Sirui Li, Mi Zhou, Sarah Entwistle, Tristan De Buysscher, Ashley Morrison, Gabriela Herrera, Cameron Harris, Benjamin G Vincent and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports. Medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.1field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 63 citations in OpenAlex.

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  20. Pancreatic Cancer Immunotherapy: A Team-Based Approach.Cancer treatment and research · 2025
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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

15 authors at 1 institution in 1 country.

Bhalchandra MirlekarLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Yan WangLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Sirui LiLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Mi ZhouLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Sarah EntwistleLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Tristan De BuysscherBioinformatics and Analytics Research Collaborative, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Ashley MorrisonLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Gabriela HerreraLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Cameron HarrisLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Benjamin G VincentLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA; Department of Microbiology and Immunology, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Jenny P-Y TingLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA; Department of Microbiology and Immunology, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA; Department of Genetics, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Naim RashidLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA; Department of Biostatistics, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
William Y KimLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA; Department of Medicine-Oncology, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Jen Jen YehLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA; Department of Surgery, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Yuliya Pylayeva-GuptaLineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA; Department of Genetics, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA. Electronic address: yuliyap1@email.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI David Darr · 1985 to 2026
$201.5M
Intracellular Innate Immune Receptors in Cancer Suppression and ImmunotherapyR35CA232109 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TING, JENNY P · 2019 to 2025
$6.4M
Function of IL35+ B cells in pancreatic cancerR37CA230786 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PYLAYEVA-GUPTA, YULIYA · 2019 to 2025
$3.0M
NCI NIH HHS P30 CA016086NCI NIH HHS R35 CA232109NCI NIH HHS R37 CA230786
6 · The paper itself

Abstract

Plasma cell responses are associated with anti-tumor immunity and favorable response to immunotherapy. B cells can amplify anti-tumor immune responses through antibody production; yet B cells in patients and tumor-bearing mice often fail to support this effector function. We identify dysregulated transcriptional program in B cells that disrupts differentiation of naive B cells into anti-tumor plasma cells. The signaling network contributing to this dysfunction is driven by interleukin (IL) 35 stimulation of a STAT3-PAX5 complex that upregulates the transcriptional regulator BCL6 in naive B cells. Transient inhibition of BCL6 in tumor-educated naive B cells is sufficient to reverse the dysfunction in B cell differentiation, stimulating the intra-tumoral accumulation of plasma cells and effector T cells and rendering pancreatic tumors sensitive to anti-programmed cell death protein 1 (PD-1) blockade. Our findings argue that B cell effector dysfunction in cancer can be due to an active systemic suppression program that can be targeted to synergize with T cell-directed immunotherapy.

Indexed as

Pancreatic NeoplasmsProgrammed Cell Death 1 ReceptorAnimalsInterleukinsLymphocyte ActivationMicePlasma CellsInterleukinsProgrammed Cell Death 1 Receptoranti-tumor immunityBcl6pancreatic cancerplasma cellsregulatory B cells

Identifiers

PMID36099917
PMCPMC9512696
OpenAlexW4295755824

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.