What question did this study set out to answer?

This study aims to investigate the effects of chidamide on AML-associated macrophages and its underlying mechanisms.

December 8, 2025BloodOpen Access

Chidamide reprograms AML-associated macrophages via HDAC3 inhibition to boost CD8+ T cell immunity

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Authors

TZTan Zhili YZYaling Zheng

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Overview

Experimental evidence demonstrates that chidamide reprograms macrophages and boosts CD8+ T cell immunity in acute myeloid leukemia, indicating a potential immunotherapy approach.

Key Points

This study aims to investigate the effects of chidamide on AML-associated macrophages and its underlying mechanisms.
Analyzed scRNA-seq and transcriptome datasets to evaluate gene expression patterns in AML.
Established AML-educated macrophage model and measured immune markers post-chidamide treatment using qRT-PCR.
Conducted co-culture with CD8+ T cells and evaluated proliferation via flow cytometry.
Utilized RNA sequencing to identify core regulatory pathways and performed in vivo experiments with AML models.
Chidamide treatment converted macrophages to an immune-activated phenotype, increasing markers like CD80 and IL-6.
Chidamide reversed the suppressive effect of AAMs on CD8+ T cell proliferation.
In vivo treatment led to significant tumor growth suppression and increased M1 macrophage infiltration.
Activation of the TNF-α/NF-κB pathway was crucial for chidamide's immune-activated effects, confirmed by TNF-α inhibitor studies.

Cite This Study

Zhili et al. (2025) studied this question.

synapsesocial.com/papers/69362f604fa91c937236dcdb https://doi.org/10.1182/blood-2025-1494

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December 8, 2025BloodOpen Access

Chidamide reprograms AML-associated macrophages via HDAC3 inhibition to boost CD8+ T cell immunity

View Full Paper

Ask AI

Bookmark

Authors

TZTan Zhili YZYaling Zheng

Discussion

Member takes

Overview

Experimental evidence demonstrates that chidamide reprograms macrophages and boosts CD8+ T cell immunity in acute myeloid leukemia, indicating a potential immunotherapy approach.

Key Points

This study aims to investigate the effects of chidamide on AML-associated macrophages and its underlying mechanisms.
Analyzed scRNA-seq and transcriptome datasets to evaluate gene expression patterns in AML.
Established AML-educated macrophage model and measured immune markers post-chidamide treatment using qRT-PCR.
Conducted co-culture with CD8+ T cells and evaluated proliferation via flow cytometry.
Utilized RNA sequencing to identify core regulatory pathways and performed in vivo experiments with AML models.
Chidamide treatment converted macrophages to an immune-activated phenotype, increasing markers like CD80 and IL-6.
Chidamide reversed the suppressive effect of AAMs on CD8+ T cell proliferation.
In vivo treatment led to significant tumor growth suppression and increased M1 macrophage infiltration.
Activation of the TNF-α/NF-κB pathway was crucial for chidamide's immune-activated effects, confirmed by TNF-α inhibitor studies.

Cite This Study

Zhili et al. (2025) studied this question.

synapsesocial.com/papers/69362f604fa91c937236dcdb https://doi.org/10.1182/blood-2025-1494

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