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Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018
Macrophage NPM1 drives anti-tumor immunity via the STAT3-CCRL2 axis
Lei Hong1,2, Yue Yang2,3, Yuwen Han1,2
1School of Biomedical Engineering (Suzhou), Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Frontiers in Immunology
|August 6, 2026
Summary
Nucleophosmin (NPM1) regulates anti-tumor immunity by controlling macrophage polarization and T cell function. NPM1 deficiency promotes tumor growth, while its overexpression enhances anti-tumor responses.
Area of Science:
- Immunology
- Oncology
- Molecular Biology
Background:
- Nucleophosmin (NPM1) is a known oncogene in acute myeloid leukemia.
- Its role in solid tumor immunity is less understood.
- This study investigates NPM1's function in the tumor microenvironment.
Purpose of the Study:
- To elucidate the role of NPM1 in regulating anti-tumor immunity.
- To understand NPM1's mechanism of action in solid tumors.
Main Methods:
- Flow cytometry to analyze immune cell populations (macrophages, T cells).
- RNA-sequencing to identify downstream NPM1 targets.
- Chromatin immunoprecipitation and luciferase assays to study NPM1-STAT3 interaction.
Main Results:
- NPM1 deficiency accelerated tumor growth in mouse models (colon and lung cancer).
- Lack of NPM1 led to increased immunosuppressive M2-like tumor-associated macrophages (TAMs) and impaired CD8+ T cell function.
- NPM1 binds to STAT3, promoting CCRL2 transcription, a key factor in macrophage polarization.
- NPM1 overexpression suppressed tumor growth and enhanced anti-tumor immunity.
Conclusions:
- NPM1 plays a protective role against tumor progression.
- NPM1 regulates TAM polarization and T cell function through the STAT3-CCRL2 pathway.
