Macrophages are among the most abundant immune cells in the lung tumor microenvironment (TME). They shape tumor initiation, progression, immune escape, and response to modern therapies such as immune checkpoint inhibitors and targeted agents. In both non–small cell lung cancer (NSCLC) and small-cell lung cancer (SCLC), tumor-associated macrophages (TAMs) are now recognized as key orchestrators of an immunosuppressive niche and powerful predictors of outcome.

Creative Biolabs offers an integrated toolbox—from primary macrophage isolation and polarization assays to advanced co-culture systems, multi-omics profiling, and in vivo lung cancer models.

Overview of Macrophages in Lung Cancer

Healthy lung tissue hosts a complex and layered macrophage network:

• Alveolar macrophages (AMs) reside on the luminal side of alveoli, acting as frontline sentinels that clear particulates, pathogens, and apoptotic cells while maintaining gas-exchange homeostasis.
• Interstitial macrophages (IMs) are embedded within the lung parenchyma, interacting closely with fibroblasts, endothelial cells, and lymphocytes to tune tissue remodeling and local immunity.
• Monocyte-derived macrophages (MDMs) are recruited from the circulation during inflammation, infection, or tumor development, where they differentiate into context-specific phenotypes.

In lung cancer, all three compartments—alveolar, interstitial, and monocyte-derived macrophages—converge within or around tumor lesions. Their proportion, spatial organization (tumor islets vs stroma vs perivascular regions), and functional polarization strongly influence tumor evolution and patient prognosis.

Making up the majority of the immune infiltrate in tumor, macrophages are a key cell type related to cancer and are believed to play an important role in the growth, progression, and metastasis of tumors. TAMs play an important role in lung cancer initiation and progression. They provide a suitable microenvironment to support growth, immunosuppression, invasion, and therapeutic resistance in lung cancer, primarily by secreting transforming growth factor-beta (TGF-β), interleukin (IL)-10, CC chemokine ligand 18 (CCL18), matrix metalloproteases (MMPs), vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2) and platelet-derived growth factor (PDGF).

Fig.1 Roles of tumor-associated macrophages (TAMs) in the microenvironment of lung cancer.^1,2

Rather than static subtypes, TAMs in lung cancer are now viewed as dynamic populations traversing a spectrum of states. Temporal studies emphasize that early-stage tumors may harbor more inflammatory macrophages, while advanced lesions are dominated by M2-like, immunoregulatory phenotypes that blunt anti-tumor immunity.

Our Lung Cancer–Focused Macrophage Service Portfolio

Deciphering macrophage biology in lung cancer demands integrated, disease-relevant models and high-resolution analytics. Creative Biolabs provides a comprehensive, modular service portfolio tailored to lung cancer research and drug discovery. We combine specialized macrophage platforms with lung tumor models to help you:

• Quantify and phenotype TAMs across disease stages and treatment conditions.
• Model macrophage–tumor–stroma crosstalk in physiologically relevant settings.
• Evaluate novel agents targeting macrophage recruitment, polarization, or function.

TAM Profiling in Lung Samples

We support deep characterization of macrophage populations in:

• Fresh or frozen tumor tissue, adjacent non-tumor tissue.
• Bronchoalveolar lavage (BAL) samples for alveolar macrophage profiling.
• Peripheral blood mononuclear cells (PBMCs) to track circulating monocytes and macrophage precursors.
• Syngeneic, orthotopic, or genetically engineered mouse models of lung cancer.
• Humanized mouse systems and PDX models capturing patient-specific immune contexts.

Typical readouts include:

• Multiparameter flow cytometry panels for M1/M2 markers (e.g., CD68, CD80, CD86, HLA-DR, CD163, CD206, PD-L1).
• Immunohistochemistry (IHC) and immunofluorescence (IF) to map TAM spatial distribution (tumor islets vs stroma vs perivascular).
• Transcriptomic and seq profiling to dissect macrophage states, lineage origin (TRM vs MDM), and pathway activity.

Macrophage Polarization & Functional Assays Under Lung TME Conditions

We design in vitro systems that mirror the unique environment of lung tumors. Macrophage sources include macrophages derived from human PBMCs (inducible by M-CSF and GM-CSF), macrophages derived from induced pluripotent stem cells (iPSCs), myeloid cell lines, and rodent macrophages used for mechanistic studies and preclinical screening.

We provide polarization strategies and functional analyses.

• Canonical M1 (LPS/IFN-γ) and M2 (IL-4/IL-13, IL-10) conditions for baseline benchmarking.
• Lung cancer–mimetic cocktails.
• Cytokine and chemokine profiling (IL-6, IL-10, TNF-α, TGF-β, CCL2, CXCL8, VEGF).
• Phagocytosis and efferocytosis assays (tumor cell uptake, apoptotic cell clearance).
• Antigen-presenting capacity and T-cell activation assays.

Macrophage–Tumor & Macrophage–Stromal Crosstalk Models

Lung tumors are multicellular ecosystems. We can engineer co-culture and 3D models capturing key interactions.

• Macrophage–tumor co-cultures: 2D and 3D co-culture of macrophages with NSCLC/SCLC cell lines, organoids, or tumor explants.
• Macrophage–endothelial/fibroblast co-cultures
• Triculture and organ-on-chip models: Incorporation of lung epithelial cells, macrophages, and T cells to study immune checkpoint dynamics and combination immunotherapies.

Macrophage-Targeted Screening & Biomarker Discovery

We help you prioritize candidates and biomarkers with macrophage-centric strategies.

• Hit identification and screening: Assess small molecules, biologics, nanoparticles, gene therapies, or cellular products for their ability to modulate TAM recruitment, survival, or polarization.
• Mechanistic elucidation: Interrogate signaling pathways (NF-κB, JAK/STAT, PI3K/AKT, β-catenin, PPARγ) underlying TAM reprogramming and immunosuppression.
• Biomarker strategy: Define macrophage-related gene signatures, protein panels, or imaging markers correlated with treatment response or resistance in NSCLC.

Our Integrated Platforms & Assays

To support sophisticated macrophage research in lung cancer, Creative Biolabs operates an integrated technology stack.

Therapeutic Strategies Targeting Macrophages in Lung Cancer

Given their central role in tumor progression and immune evasion, macrophages are increasingly targeted in lung cancer drug development. We design studies to explore and optimize these strategies.

• Inhibiting Macrophage Recruitment: Monocyte recruitment to lung tumors is governed by chemokines (CCL2, CCL5, CX3CL1) and growth factors (CSF-1/M-CSF).
• Therapeutic Macrophage Depletion: Depletion approaches aim to clear tumor-supportive macrophages while preserving beneficial immune functions.
• Reprogramming TAMs Toward Anti-Tumor States: Because macrophages are highly plastic, reprogramming strategies are particularly attractive. We support phenotypic and molecular assessment of reprogramming, including changes in cytokine production, T-cell priming, and tumor killing.
• Macrophage-Targeted Drug Delivery: Macrophages naturally home to hypoxic and poorly perfused tumor regions, including those deep within lung lesions.
• Combination With Immune Checkpoint Inhibitors and Targeted Agents: TAM-modulating agents plus anti-PD-1/PD-L1 or anti-CTLA-4 to overcome primary or acquired resistance in NSCLC. Macrophage-directed strategies combined with EGFR/ALK inhibitors to mitigate TKI resistance driven by an immunosuppressive, pro-angiogenic niche.

We build bespoke study designs to reveal synergy, antagonism, or sequential benefits in macrophage-rich lung cancer models.

Related Products

Below is an example of macrophage-related products that can support lung cancer research. For a full, up-to-date list, please refer to our product catalog.

Scientific Resources

Q & A

Q: Which macrophage model is most appropriate for my lung cancer project—alveolar, interstitial, or monocyte-derived macrophages?

A: The ideal model depends on your biological question. If you are studying early immune sensing, inhaled agents, or airway-focused toxicity, human alveolar macrophages or BAL-derived cells are particularly relevant. For stromal remodeling, angiogenesis, and deep parenchymal lesions, interstitial and tumor-associated macrophages from lung tissue are more informative. For screening and mechanistic studies, MDMs offer scalability and flexibility.

Q: Can you analyze macrophage subsets from our own NSCLC or SCLC samples, including archived tissue blocks?

A: Yes. When working with archived material, we optimize antibody panels and extraction protocols to maximize data yield.

Q: How do I initiate a macrophage-focused lung cancer project with Creative Biolabs, and what is the typical turnaround time?

A: Simply contact our team with a brief description of your project. We will schedule a confidential consultation with our macrophage and oncology experts to refine objectives, propose experimental strategies, and outline suitable platforms. Turnaround time depends on project scope and model complexity. For in vivo and multi-omics programs, we provide a detailed, customized timeline and regular progress updates.

Q: How do you quantify successful TAM reprogramming in your assays?

A: We take a multidimensional approach. At the surface marker level, we monitor changes in M1-associated molecules and M2-associated markers. Functionally, we track cytokine and chemokine shifts, antigen presentation, phagocytic capacity, and support for T-cell proliferation and effector function. On the metabolic side, we examine glycolytic vs oxidative profiles.

Creative Biolabs delivers an end-to-end macrophage toolset for lung cancer—spanning discovery, mechanism-of-action studies, and translational biomarker development. Tell us about your goals, and our scientists will co-design a macrophage-centered program that accelerates your path from concept to decision-ready data.

Reference

1. Liu, Lei, et al. "Targeting tumor-associated macrophage: an adjuvant strategy for lung cancer therapy." Frontiers in immunology 14 (2023): 1274547. https://doi.org/10.3389/fimmu.2023.1274547
2. Distributed under Open Access license CC BY 4.0, without modification.