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Updated: Aug 6, 2026

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Multiplex Immunohistochemical Analysis of the Spatial Immune Cell Landscape of the Tumor Microenvironment
Published on: August 18, 2023
Decoding NETosis-associated immune dysregulation in diffuse large B-cell lymphoma through integrative multi-omics and
Hanbing Yao1, Gangfeng Wang1, Yingmin Liang1
1Hematology Laboratory, Xi'an International Medical Center Hospital, Xi'an, Shaanxi, China.
Frontiers in Cell and Developmental Biology
|July 17, 2026
Summary
This study reveals a new NETosis-related gene signature that improves prognosis prediction in diffuse large B-cell lymphoma (DLBCL). The findings highlight the role of neutrophils and myeloid cells in DLBCL immune dysregulation and offer potential therapeutic targets.
Area of Science:
- Immunology
- Oncology
- Genomics
Background:
- Diffuse large B-cell lymphoma (DLBCL) is a complex cancer with poorly understood immune dysregulation.
- The role of NETosis, a neutrophil immune process, in DLBCL's tumor microenvironment and patient outcomes is unclear.
Purpose of the Study:
- To investigate the immunological impact of NETosis-related genes (NETosis-RGs) in DLBCL.
- To develop a prognostic model for DLBCL patients based on NETosis-RGs.
Main Methods:
- Utilized a multi-omics and machine learning approach to identify and analyze NETosis-RGs.
- Employed Random Survival Forest (RSF) for risk stratification and single-cell transcriptomics to map the immune landscape.
- Investigated ceRNA networks and m6A regulators for post-transcriptional and epigenetic insights.
Main Results:
- A five-gene NETosis-RG model (AKT1, SLC25A37, FPR2, TLR7, F3) effectively stratified DLBCL patients into high- and low-risk groups.
- These genes are primarily expressed in monocytes and M1 macrophages, influencing the tumor microenvironment's immune state.
- Identified multi-layered regulatory mechanisms including m6A modifications and ceRNA axes.
Conclusions:
- A novel NETosis-centered immune signature refines DLBCL prognostic stratification.
- Provides mechanistic insights into myeloid cell-driven immune dysregulation in DLBCL.
- Offers a foundation for developing immunomodulatory biomarkers and precision therapies.
