Macrophages in Glioblastoma

Overview Our Service Assays Therapeutic Strategies Workflow Advantages Related Products Scientific Resources Q & A

Glioblastoma (GBM) is among the most aggressive human cancers, defined not only by rapid growth and diffuse invasion, but also by a profoundly immunosuppressive tumor microenvironment (TME). A major architect of that microenvironment is the glioblastoma-associated myeloid compartment—tumor-associated macrophages (TAMs) and resident microglia—often representing a remarkably large fraction of tumor cellularity and shaping therapy response through cytokines, metabolic programs, and immune checkpoint crosstalk.

Creative Biolabs provides end-to-end macrophage-centric GBM study services spanning model development, phenotyping, functional assays, TAM reprogramming, and advanced single-cell/spatial readouts. Our team can align the right assays, models, and analytical depth to your milestones.

Why Macrophage-Centered GBM Research Is Now a Competitive Advantage

Unlike many solid tumors where T-cell infiltration is the primary immunology focus, GBM is frequently characterized by high myeloid infiltration and strong myeloid-driven immune suppression. Multiple studies and reviews report that TAMs/microglia can constitute ~30–50% of the tumor mass or a substantial portion of the stromal/immune compartment, making them one of the most targetable levers in GBM biology.

Single-cell studies show distinct, context-dependent microglia-like, monocyte-derived macrophage-like, and border-associated macrophage programs with spatial organization across tumor core, hypoxic niches, and invasive margins.

Fig.1 The role of tumor-associated macrophages in the progression of glioblastoma multiforme (GBM). (Grégoire, Hélène, et al., 2020)Fig.1 TAMs activities in GBM progression.1,2

Creative Biolabs' Macrophage Services for GBM

You can engage a single assay module or build a complete package that runs from model setup to mechanism-ready deliverables.

Study Strategy & Experimental Architecture

We start by aligning biology to your milestone:

  • Target class and intended MOA (CSF1R/CCR2 axis, CD47–SIRPα, CD40/TLR, metabolic reprogramming, nanoparticle delivery, etc.)
  • Model choice and translational intent (cell line vs patient-derived vs organoid; syngeneic vs xenograft)
  • Primary endpoints (phenotype shift, phagocytosis restoration, recruitment blockade, survival proxy endpoints, synergy with T cell cytotoxicity)
  • Assay depth selection

Microglia & Macrophage Sourcing, Differentiation, and Quality Control

We offer standardized and customized options:

  • Cell sources (choose one or mix): Human PBMC-derived monocyte-to-macrophage differentiation, human iPSC-derived microglia-like cells (for brain-relevant programs), mouse bone marrow-derived macrophages (BMDMs), cell-line-derived macrophage models (e.g., THP-1) for scalable screening, tumor-conditioned macrophages (GBM-CM or co-culture-induced).
  • QC and release testing options: Identity & purity (flow cytometry marker panels), viability, morphology, baseline cytokine secretion, functional readiness (phagocytosis baseline; response to polarization stimuli)

GBM-Relevant In Vitro and 3D Co-Culture Model Development

  • 2D co-culture systems (fast iteration, mechanistic clarity): Macrophage-GBM cell line co-culture, macrophage-glioma stem-like cell co-culture, transwell formats to separate contact vs soluble-factor effects, time-course designs to capture early vs late reprogramming
  • 3D spheroids & matrix-embedded invasion models (GBM realism): GBM spheroids embedded in ECM mimetics (invasion edge readouts), macrophage infiltration tracking into spheroid cores, live imaging options for migration/invasion kinetics
  • Patient-relevant GBM organoid co-culture (translational depth): Integration of macrophages/microglia into GBM organoid systems, hypoxia-gradient tuning and necrotic core modeling, optional incorporation of T cells for immune tri-culture studies
  • Microfluidic and barrier-informed platforms (advanced GBM context): flow-enabled co-culture for recruitment dynamics, perivascular niche simulation modules, optional BBB-like interfaces to evaluate trafficking/penetration concepts (R&D design)

Our Other Featured Services

If you are interested, please feel free to contact us or send us your inquiry or question.

Core Assay Modules for GBM Macrophage Studies

Module Core Assay Description
Macrophage Phenotyping & State Mapping Flow cytometry, multiparameter immunophenotyping
  • Lineage and activation panels (customizable)
  • Microglia-vs-MDM-informed marker logic when applicable
  • Quantification of state shifts after treatment
Multiplex immunofluorescence / IHC
  • Density mapping of TAMs across tumor-like compartments
  • Co-localization with tumor markers, hypoxia markers, vasculature markers
  • Optional digital pathology quantification and spatial statistics
RNA sequencing of myeloid cells
  • High-resolution state decomposition of microglia-like and macrophage-like clusters
  • Trajectory inference (activation paths under therapy pressure)
  • Candidate biomarker extraction and signature scoring
Spatial transcriptomics
  • Niche-specific TAM programs (core vs edge vs perivascular vs hypoxic)
  • Linking macrophage states to tumor cell programs and therapy resistance patterns
Functional Macrophage Assays Phagocytosis and "don't-eat-me" pathway evaluation
  • Bead-based and cell-based phagocytosis assays
  • Tumor-cell phagocytosis recovery under CD47/SIRPα-axis interventions (custom designs)
  • Quantification of engulfment index, kinetics, and durability
Efferocytosis and debris clearance under therapy-like stress
  • Apoptotic body uptake assays (TMZ/radiation mimetic contexts)
  • Resolution vs chronic inflammation signatures
Cytokine and chemokine profiling
  • Multiplex panels (IL-10, TGF-β pathway proxies, CXCL/CCl axes, pro-angiogenic factors)
  • Time-series sampling to capture transient vs stable shifts
Migration, recruitment, and invasion support assays
  • Transwell chemotaxis (CCL2/CCR2-driven recruitment logic)
  • Microfluidic gradient migration for high-content kinetics
  • Tumor invasion modulation readouts (spheroid edge expansion, ECM degradation proxies)
Antigen presentation and T-cell interaction modules
  • MHC-II/co-stimulation panels and functional activation readouts
  • Tri-culture systems to quantify whether macrophage reprogramming restores T cell activity
  • Cytotoxicity proxies and cytokine signatures in co-culture
Metabolic and stress-state profiling
  • Seahorse-style bioenergetics or targeted metabolic assays (project-dependent)
  • Hypoxia-conditioned macrophage function mapping
  • Linking metabolic signatures to immunosuppressive programs
TAM Reprogramming & Macrophage-Targeting Therapeutics Support Mechanism-driven screening designs
  • CSF1R-axis perturbation (reprogramming vs depletion logic)
  • Recruitment blockade concepts (chemokine axis-informed approaches)
  • Innate activation strategies (CD40/TLR logic; project-dependent)
  • Combination strategies: macrophage reprogramming + checkpoint blockade concepts (R&D evaluation and hypothesis testing)

TAM-targeted Therapeutics in GBM

There are several strategies of therapies targeting TAMs:

  • Targeting TAMs to block their recruitment to the tumor site. It can be achieved by targeting the CCL2/chemokine receptor 2 (CCR2) axis. CCL2 is an inflammatory chemokine that can recruit macrophages and Treg lymphocytes leading to an immunosuppressive environment.
  • Reprogramming of TAMs toward an antitumoral phenotype: 1) Inhibition of CD47: CD47 expressed by cancer cells inhibits phagocytosis through its interaction with signal regulatory protein-a (SIRPa) expressed by macrophages thus sending out a "do not eat me" signal; 2) Activation of CD40: CD40 is expressed on monocytes, macrophages, dendritic cells, and B cells and belongs to the TNF receptor superfamily. Targeting CD40 modulated the immune cell number and led to an antitumor response; 3) Toll-like receptors (TLRs) Agonist: TLRs are normally activated by microbial moieties (including nucleic acids) allowing macrophages to acquire an M1 phenotype.
  • Depletion of TAMs. The activation of TAMs is dependent on the CSF1R signaling pathway. Against CSF1R signaling pathway and bisphosphonates are two ways to deplete the number of TAMs in the tumor.

Based on our powerful Macrophage Therapeutics Development Platform designed specifically to meet our clients' challenging requirements, Creative Biolabs offers extremely useful and valuable biotechnological services for macrophage development projects, and we embrace your mission as our own.

Workflow: How We Run a GBM Macrophage Project

  • Scientific alignment call (targets, hypothesis, endpoints, constraints)
  • Model selection & feasibility (2D/3D/organoid; source cells; controls)
  • Assay design & panel finalization (markers, readouts, timepoints)
  • Execution & QC checkpoints (viability, reproducibility, acceptance criteria)
  • Bioinformatics & interpretation (especially for single-cell/spatial projects)
  • Delivery & next-step planning (decision memo + optional follow-up study design)

Why Choose Creative Biolabs for GBM Macrophage Studies

  • Macrophage-first infrastructure: service ecosystem built around macrophage biology, not a generic "add-on" immunology menu
  • GBM-aware assay design: microglia/TAM distinctions, hypoxia conditioning, invasion-edge context
  • Flexible depth: from fast screening to single-cell/spatial atlasing
  • Mechanism-forward reporting: we connect phenotype shifts to functional consequences and development decisions
  • One team, end-to-end: fewer handoffs, cleaner accountability, faster iteration

Related Products

Creative Biolabs will provide tailored research solutions for specific projects and offer high-quality, complementary research tools.

Cat.No Product Name Product Type
MTS-1022-JF1 B129 Mouse Bone Marrow Monocytes, 1 x 10^7 cells Mouse Monocytes
MTS-0922-JF99 Human M0 Macrophages, 1.5 x 10^6 Human M0 Macrophages
MTS-0922-JF52 C57/129 Mouse Macrophages, Bone Marrow C57/129 Mouse Macrophages
MTS-1022-JF6 Human Cord Blood CD14+ Monocytes, Positive selected, 1 vial Human Monocytes
MTS-0922-JF34 CD1 Mouse Macrophages CD1 Mouse Macrophages
MTS-1123-HM6 Macrophage Colony Stimulating Factor (MCSF) ELISA Kit, Colorimetric Detection Kit
MTS-1123-HM15 Macrophage Chemokine Ligand 19 (CCL19) ELISA Kit, qPCR Detection Kit
MTS-1123-HM17 Macrophage Chemokine Ligand 4 (CCL4) ELISA Kit, Colorimetric Detection Kit
MTS-1123-HM49 Macrophage Migration Inhibitory Factor (MIF) ELISA Kit, Colorimetric Detection Kit
MTS-1123-HM42 Macrophage Receptor with Collagenous Structure ELISA Kit, Colorimetric Detection Kit

Scientific Resources

Q & A

Q: We're early-stage—can you help us choose the right GBM model for macrophage work?

A: Yes. We routinely help clients decide between 2D co-cultures (fast MOA signals), 3D spheroids (infiltration/invasion realism), organoids (translational depth), and advanced barrier/flow concepts. We'll recommend a model based on your target class, expected macrophage mechanism, timeline, budget, and the type of data your stakeholders need.

Q: Can you distinguish microglia from infiltrating macrophages in our readouts?

A: We can design lineage-aware strategies using validated marker logic and appropriate caveats. Published analyses show that markers such as P2RY12 and TMEM119 can discriminate microglia from TAMs in GBM, while other markers can be context-dependent—so we typically use multi-marker approaches and confirm with functional and/or transcriptomic signatures when needed.

Q: What sample types do you accept?

A: Yes. Using your own tumor cells often strengthens program continuity. We'll align culture conditions, labeling strategy, and co-culture design to preserve the biology you care about while ensuring the macrophage component remains interpretable and reproducible.

Q: What kind of data and reports will we receive from your services?

A: Our reports are designed to be actionable and decision-oriented. Depending on your service selection, you will receive: raw data files, analysis summaries with statistical analysis, biomarker identification, detailed figures for publication-ready visual representation and interpretation/conclusion.

Ready to build a macrophage-centered GBM study plan that is truly mechanism-driven? Creative Biolabs will respond with a project-specific study design and a clear, milestone-aligned quotation.

Reference

  1. Grégoire, Hélène, et al. "Targeting tumor associated macrophages to overcome conventional treatment resistance in glioblastoma." Frontiers in pharmacology 11 (2020): 368. https://doi.org/10.3389/fphar.2020.00368
  2. Distributed under Open Access license CC BY 4.0, without modification.
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