Evidence map›Paper›PMID 35523809›Full record

ArticleNature communications2022

The immune checkpoint B7x expands tumor-infiltrating Tregs and promotes resistance to anti-CTLA-4 therapy.

Peter John, Marc C Pulanco, Phillip M Galbo, Yao Wei, Kim C Ohaegbulam, Deyou Zheng, Xingxing Zang

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.4field-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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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  12. Multimodal cell-cell communication driving CD8Frontiers in immunology · 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

7 authors at 1 institution in 1 country.

Peter JohnDepartment of Microbiology & Immunology, Albert Einstein College of Medicine, Bronx, NY, United States.
Marc C PulancoDepartment of Microbiology & Immunology, Albert Einstein College of Medicine, Bronx, NY, United States.
Phillip M GalboDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.
Yao WeiDepartment of Microbiology & Immunology, Albert Einstein College of Medicine, Bronx, NY, United States.
Kim C OhaegbulamDepartment of Microbiology & Immunology, Albert Einstein College of Medicine, Bronx, NY, United States.
Deyou ZhengDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.ORCID 0000-0003-4354-5337
Xingxing ZangDepartment of Microbiology & Immunology, Albert Einstein College of Medicine, Bronx, NY, United States. xingxing.zang@einsteinmed.edu.ORCID 0000-0001-5380-1942
Albert Einstein College of Medicine · US

Funding

CTSA Administrative Supplement for Informatics Core: A novel AI/ML system to predict respiratory failure and ARDS in Covid-19 patientsUL1TR002556 · NCATS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI KELLER, MARLA J, KIM, MIMI Y · 2018 to 2022
$26.7M
Tumor-expressed immune checkpoint B7x-mediated resistance to anti-CTLA-4 therapy.R01CA175495 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI ZANG, XINGXING · 2014 to 2025
$5.1M
NRSA Training CoreTL1TR002557 · NCATS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI MARANTZ, PAUL R · 2018 to 2022
$1.0M
B7x in Cancer: Mechanisms and TherapiesF30CA224931 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI JOHN, PETER · 2018 to 2021
$201k
NCATS NIH HHS TL1 TR002557NCATS NIH HHS UL1 TR002556NCI NIH HHS F30 CA224931NCI NIH HHS R01 CA175495
6 · The paper itself

Abstract

Immune checkpoint molecules play critical roles in regulating the anti-tumor immune response, and tumor cells often exploit these pathways to inhibit and evade the immune system. The B7-family immune checkpoint B7x is widely expressed in a broad variety of cancer types, and is generally associated with advanced disease progression and poorer clinical outcomes, but the underlying mechanisms are unclear. Here, we show that transduction and stable expression of B7x in multiple syngeneic tumor models leads to the expansion of immunosuppressive regulatory T cells (Tregs). Mechanistically, B7x does not cause increased proliferation of Tregs in tumors, but instead promotes the conversion of conventional CD4

Indexed as

NeoplasmsB7 AntigensHumansImmunotherapyT-Lymphocytes, RegulatoryB7 Antigens

Identifiers

PMID35523809
PMCPMC9076640
OpenAlexW4229052985

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.