Related Experiment Video
Updated: Jan 9, 2026
Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
Published on: November 28, 2015
Mapping TAM-tumor crosstalk in glioma via ligand-receptor multi-omics: mechanisms of immune evasion
Dong Zhang1,2, Yiming Ma3, Daxiong Feng1
1Department of Orthopedics, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Abstract:
Diffuse gliomas remain lethal primary brain tumors. Immune-checkpoint inhibitors have not delivered durable benefit for most patients, reflecting myeloid-dominant immunosuppression and spatially organized immune exclusion. In this mini-review we summarize ligand-receptor multi-omics-single-cell RNA/CITE-seq, single-cell chromatin accessibility, and spatial proteo-transcriptomics-that resolve microglia- and monocyte-derived TAM programs and malignant state continua, and we appraise translational opportunities spanning TAM reprogramming (CSF1-CSF1R), perivascular SPP1-CD44 disruption, and innate-adaptive combinations targeting CD47-SIRPα, CD39-CD73, and PD-1/PD-L1. We also discuss challenges-including ontogeny-aware state definitions, heteromer-aware databases, chromatin gating of receivers (requiring accessible regulatory DNA for the receptor and its program), spatial registration, and limited assay standardization-that temper implementation. By integrating myeloid-informed readouts (SPP1-TAM burden, CD39-CD73 proximity, HMOX1+ IL-10 niches, serum IL-8), emerging strategies aim to restore antigen presentation, enable effector ingress, and remodel vascular-stromal interfaces. Our synthesis provides an appraisal of reproducible communication architectures in glioma and outlines pragmatic reporting standards and trial-ready pharmacodynamic endpoints for myeloid-informed precision immuno-oncology. We hope these insights will assist researchers and clinicians as they design multi-omics pipelines and interventions to convert suppressive ecosystems into responsive ones.
Insights
Diffuse gliomas are deadly brain tumors. New multi-omics approaches reveal myeloid cell roles, offering strategies to reprogram the tumor microenvironment and improve immunotherapy effectiveness for better patient outcomes.
Area of Science:
- Neuro-oncology
- Immunology
- Multi-omics
Background:
- Diffuse gliomas are aggressive primary brain tumors with poor prognoses.
- Current immunotherapies show limited efficacy due to myeloid-dominant immunosuppression and immune exclusion.
Purpose of the Study:
- To review multi-omics single-cell technologies for characterizing tumor-associated myeloid cells (TAMs) in gliomas.
- To identify translational strategies targeting myeloid cell programs for improved glioma immunotherapy.
Main Methods:
- Summarized findings from single-cell RNA/CITE-seq, chromatin accessibility, and spatial proteo-transcriptomics.
- Appraised ligand-receptor interactions and myeloid cell states.
- Integrated myeloid-informed readouts for therapeutic targeting.
Main Results:
- Multi-omics data resolve microglia- and monocyte-derived TAM programs and malignant states.
- Identified key pathways for TAM reprogramming (CSF1-CSF1R), perivascular disruption (SPP1-CD44), and innate-adaptive combinations (CD47-SIRPα, CD39-CD73, PD-1/PD-L1).
Conclusions:
- Emerging strategies aim to restore antigen presentation, enhance effector cell infiltration, and remodel the tumor microenvironment.
- Standardized reporting and trial-ready endpoints are crucial for myeloid-informed precision immuno-oncology in glioma.
