Evidence map›Paper›PMID 29137299›Full record

ArticleOncotarget2017

Tumor-expressed immune checkpoint B7x promotes cancer progression and antigen-specific CD8 T cell exhaustion and suppressive innate immune cells.

Kim C Ohaegbulam, Weifeng Liu, Hyungjun Jeon, Steven C Almo, Xingxing Zang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. The role of CD8Heliyon · 2024
    Review
  7. Review
  8. Article
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  10. Article
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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

5 authors at 1 institution in 1 country.

Kim C OhaegbulamDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.
Weifeng LiuDepartment of Biochemistry, Albert Einstein College of Medicine, Bronx, NY, USA.
Hyungjun JeonDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.
Steven C AlmoDepartment of Biochemistry, Albert Einstein College of Medicine, Bronx, NY, USA.
Xingxing ZangDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.
Albert Einstein College of Medicine · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
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
Mechanisms and Therapies of B7x and B7-H3 in T1DR01DK100525 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI ZANG, XINGXING · 2015 to 2019
$1.9M
Tumor expressed B7x accelerates disease and is a novel target for immunotherapyF31CA183493 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI OHAEGBULAM, KIM C · 2014 to 2017
$193k
NCI NIH HHS F31 CA183493NCI NIH HHS R01 CA175495NIDDK NIH HHS R01 DK100525NIGMS NIH HHS T32 GM007288
6 · The paper itself

Abstract

B7x (B7-H4 or B7S1) is a coinhibitory member of the B7 immune checkpoint ligand family that regulates immune function following ligation with its unknown cognate receptors. B7x has limited expression on normal tissues, but is up-regulated on solid human tumors to inhibit anti-tumor immunity and associates with poor clinical prognosis. We assessed the contribution of cytokine stimuli to induce surface B7x expression on cancer cells and the role of tumor-expressed B7x in a murine pulmonary metastasis model, and finally evaluated the potential interaction between B7x and Neuropilin-1, a suggested potential cognate receptor. We showed that pro-inflammatory and anti-inflammatory cytokines IFNγ, TNFα, and IL-10 did not induce expression of B7x on human or murine cancer cells. Following i.v. injection of CT26, a murine colon cancer cell line in the BALB/c background, we observed a significant increase in tumor burden in the lung of B7x-expressing CT26 mice compared to B7x-negative parental CT26 control mice. This was marked by a significant increase in M2 tumor associated macrophages and antigen-specific CD8 T cell exhaustion. Finally, we found through multiple systems that there was no evidence for B7x and Neuropilin-1 direct interaction. Thus, the B7x pathway has an essential role in modulating the innate and adaptive immune cell infiltrate in the tumor microenvironment with its currently unknown cognate receptor(s).

Indexed as

B7xCD8 T cellsimmune checkpointinnate cellspulmonary metastases

Identifiers

PMID29137299
PMCPMC5669925
OpenAlexW2756049664

What OpenQuestion holds

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LicenceCC BY
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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.