Evidence map›Paper›PMID 35750747›Full record

ArticleBritish journal of cancer2022

Macrophage-derived CCL23 upregulates expression of T-cell exhaustion markers in ovarian cancer.

Kalika Kamat, Venkatesh Krishnan, Oliver Dorigo

Open access · greenAbstract read
In one paragraph

Article in British journal of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.7field-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

37 citing papers in PubMed, 57 citations in OpenAlex.

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  9. Transcriptomic profiling of a canine malignant eyelid melanoma.Brazilian journal of veterinary medicine · 2026
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  10. Tumor-associated macrophages and platelets in tumor microenvironment and its potential therapeutic role in ovarian cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

3 authors at 2 institutions in 1 country.

Kalika KamatDepartment of Obstetrics and Gynecology, Division of Gynecologic Oncology, Stanford Women's Cancer Center, Stanford Cancer Institute, Stanford, CA, USA.
Venkatesh KrishnanDepartment of Obstetrics and Gynecology, Division of Gynecologic Oncology, Stanford Women's Cancer Center, Stanford Cancer Institute, Stanford, CA, USA.ORCID http://orcid.org/0000-0001-9292-4515
Oliver DorigoDepartment of Obstetrics and Gynecology, Division of Gynecologic Oncology, Stanford Women's Cancer Center, Stanford Cancer Institute, Stanford, CA, USA. odorigo@stanford.edu.ORCID http://orcid.org/0000-0002-1976-5201
Stanford Cancer InstituteStanford Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMacrophages are an important component of the tumour immune microenvironment (TME) and can promote tumour growth and metastasis. Macrophage-secreted chemokine-ligand-23 (CCL23) induces ovarian cancer cell migration via chemokine-receptor 1 (CCR1). However, the effect of CCL23 on other immune cells in the TME is unknown.

methodsCCL23 levels were measured by ELISA. The expression of surface markers in exhaustion assays was quantified by flow cytometry. Signalling pathways were identified by phosphokinase array and validated by western blot.

resultsAscites from patients with high-grade serous ovarian cancer (HGSC) contain high levels of CCL23. Similarly, significantly higher CCL23 levels were found in plasma from HGSC patients compared to healthy individuals. RNA-seq analysis of ovarian cancer tissues from TCGA showed that expression of CCL23 correlated with the presence of macrophages. In tissues with high levels of CCL23 and macrophage content, the fraction of CD8 + T cells expressing exhaustion markers CTLA-4 and PD-1 were significantly higher compared to low-level CCL23 tissues. In vitro, CCL23 induced upregulation of immune checkpoint proteins on CD8 + T cells, including CTLA-4, TIGIT, TIM-3 and LAG-3 via phosphorylation of GSK3β in CD8 + T cells.

conclusionsOur data suggest that CCL23 produced by macrophages contributes to the immune-suppressive TME in ovarian cancer by inducing an exhausted T-cell phenotype.

Indexed as

Ovarian NeoplasmsTumor MicroenvironmentCarcinoma, Ovarian EpithelialChemokine CCL22Chemokines, CCCTLA-4 AntigenFemaleHumansLigandsMacrophagesCCL23 protein, humanChemokine CCL22Chemokines, CCCTLA-4 AntigenLigands

Identifiers

PMID35750747
PMCPMC9470573
OpenAlexW4283392344

What OpenQuestion holds

Textmetadata
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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.