Evidence map›Paper›PMID 39273683›Full record

ArticleInternational journal of molecular sciences2024

The Immunosuppressive Receptor CD32b Regulation of Macrophage Polarization and Its Implications in Tumor Progression.

Hong-Jing Chuang, Ying-Yin Chen, Yi-Da Chung, Evelyn Huang, Cadence Yoshang Huang, Jrhau Lung, Chung-Yu Chen, Hui-Fen Liao

Abstract read
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Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

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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

8 authors.

Hong-Jing ChuangDepartment of Pathology, National Taiwan University Hospital Yunlin Branch, Yunlin 640, Taiwan.
Ying-Yin ChenDepartment of Internal Medicine, National Taiwan University Hospital Yunlin Branch, Yunlin 640, Taiwan.
Yi-Da ChungDepartment of Biochemical Science and Technology, National Chiayi University, Chiayi 600, Taiwan.
Evelyn HuangCell and Molecular Biology, Northeastern University, Boston, MA 02115, USA.
Cadence Yoshang HuangTaipei American School, Taipei 111, Taiwan.
Jrhau LungDepartment of Medical Research and Development, Chang Gung Memorial Hospital, Chiayi Branch, Chiayi 613, Taiwan.ORCID 0000-0003-2100-3713
Chung-Yu ChenDepartment of Internal Medicine, National Taiwan University Hospital Yunlin Branch, Yunlin 640, Taiwan.ORCID 0000-0001-9002-7255
Hui-Fen LiaoDepartment of Biochemical Science and Technology, National Chiayi University, Chiayi 600, Taiwan.

Funding

National Taiwan University Hospital Yunlin Branch NTUHYL106.C003
6 · The paper itself

Abstract

Macrophages, pivotal components of the immune system, orchestrate host defense mechanisms in humans and mammals. Their polarization into classically activated macrophages (CAMs or M1) and alternatively activated macrophages (AAMs or M2) dictates distinct functional roles in immunity and tissue homeostasis. While the negative regulatory role of CD32b within the FC gamma receptor (FCγR) family is recognized across various immune cell types, its influence on macrophage polarization remains elusive. This study aimed to elucidate the regulatory role of CD32b in macrophage polarization and discern the differential expression markers between the M1 and M2 phenotypes following CD32b siRNA transfection. The results revealed a decrease in the CD32b levels in lipopolysaccharide (LPS)-treated M1 and an increase in interleukin-4 (IL-4)-treated M2 macrophages, as observed in macrophage Raw264.7 cells. Furthermore, CD32b siRNA transfection significantly downregulated the M2 markers (IL-10, VEGF, Arg-1, and STAT6), while upregulating the M1 markers (IL-6, NF-κB, NOS2, and STAT1) in the Raw264.7 cells. Similar findings were recapitulated in macrophage-rich adherent cells isolated from mouse spleens. Additionally, the cytopathological analysis of pleural effusions and ascitic fluids from patients with cancer revealed a positive correlation between advanced tumor stages, metastasis, and elevated CD32b levels. In conclusion, this study highlights the regulatory influence of CD32b in suppressing M1 expression and promoting M2 polarization. Moreover, heightened M2 activation and CD32b levels appear to correlate with tumor progression. A targeted CD32b blockade may serve as a novel therapeutic strategy to inhibit M2 macrophage polarization and is promising for anti-tumor intervention.

Indexed as

Macrophage ActivationMacrophagesReceptors, IgGAnimalsDisease ProgressionFemaleHumansInterleukin-4LipopolysaccharidesMaleMiceNeoplasmsRAW 264.7 CellsFc gamma receptor IIBInterleukin-4LipopolysaccharidesReceptors, IgGalternatively activated macrophage (M2)classically activated macrophage (M1)FC gamma receptor CD32bmacrophage polarizationtumor stage

Identifiers

PMID39273683
PMCPMC11395990

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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.