Macrophages sit at the hub of innate–adaptive crosstalk. In autoimmune settings such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and multiple sclerosis (MS), skewed polarization, defective efferocytosis, metabolic rewiring, and tissue-specific macrophage programs amplify chronic inflammation and tissue damage. Creative Biolabs builds disease-relevant, modular assays to quantify these macrophage states and their functional consequences—so you can validate mechanisms, rank candidates, and make confident go/no-go decisions.

Macrophage Polarization in Autoimmune Diseases

Macrophages infiltration is generally observed in many autoimmune diseases. Characteristic M1 pro-inflammatory profile is beneficial for pathogens/tumor elimination but is detrimental for the wound healing process. In contrast, M2 anti-inflammatory profile improves chronic inflammatory diseases and regeneration. Moreover, 'chimeric' M1-M2 macrophages with mixed phenotypic features have been described in certain autoimmune diseases. Many diseases are correlated with an altered balance of M1/M2 macrophage phenotypes. Several autoimmune diseases are correlated with an increased M1/M2 ratio. Likely, a reduced frequency of anti-inflammatory M2 macrophages or prolonged activation of M1 macrophages could be implicated in the development of detrimental inflammation and autoimmunity. Additionally, it is known that the deleterious effects of reactive oxygen species produced by M1 macrophages can play a vital role by inducing the cycle of damage and healing during an autoimmune process.

Fig.1 Modulation of autoimmune diseases by monocytes and macrophages.^1,2

What We Offer

Creative Biolabs offers a comprehensive macrophage-autoimmune disease research solution centered on the objectives of disease relevance, mechanism-driven insights, and data-driven translation.

Disease-Relevant Model Library

• Human PBMC-derived monocyte → M0 → M1/M2 polarization, mouse BMDM/peritoneal macrophages, THP-1 and RAW264.7 lines
• Tissue-context models: synovial-like macrophages (RA), renal-associated macrophages/LN models (SLE), microglia/CNS-infiltrating macrophages (MS)
• Microenvironment modules: macrophage–T cell/fibroblast/epithelial co-culture, hypoxia, lactate, iron loading, immune complexes

Physiologic Stimuli & Interventions

• TLR ligands (e.g., LPS, R848, CpG), Th1/Th2/Th17 cytokines (IFN-γ, TNF-α, IL-4, IL-10, etc.)
• Autoimmune-relevant inputs: immune complexes, dsDNA/nucleosomes (SLE), myelin/OPC debris (MS), citrullinated/modified proteins and synovial factors (RA)
• Assay-ready evaluation of small molecules, antibodies/biologics, and nano-delivery systems

Multi-Modal Readouts

• Phenotype & function: flow panels; phagocytosis & ADCP; efferocytosis; chemotaxis/migration; antigen presentation (MHC-II/co-stimulatory molecules)
• Cytokines & signaling: ELISA; NF-κB/STAT/IRF reporters; NLRP3 inflammasome activation
• Metabolism & transcription: ECAR/OCR; qPCR/RNA-seq; targeted metabolomics/lipidomics
• Co-culture effects: T-cell proliferation/differentiation, fibroblast ECM signatures, myelin processing/clearance (MS)

Creative Biolabs provides a full range of professional services for macrophage development projects with our highly experienced team. We provide the wonderful one-stop platform to advance our global clients' projects.

For more information on the role of macrophage in autoimmune diseases, please click on the links below.

• Macrophages in Rheumatoid Arthritis (RA)
• Macrophages in Inflammatory Bowel Disease (IBD)
• Macrophages in Multiple Sclerosis (MS)
• Macrophages in Systemic Lupus Erythematous (SLE)
• Macrophages in Type 1 Diabetes (T1D)

Workflow

Therapeutic Strategies Targeting Macrophages

Given their central role in autoimmune diseases, a variety of therapeutic strategies targeting macrophages are under active investigation and development.

• Inhibiting Macrophage Recruitment: Blocking key chemokines and their receptors, such as the CCL2-CCR2 or CX3CL1-CX3CR1 axes, can reduce the migration of monocytes from the bloodstream into inflamed tissues, thereby lowering the local macrophage population. Several small-molecule CCR2 antagonists have entered clinical trials.
• Depleting Pathogenic Macrophages: Using antibody-drug conjugates (ADCs) or immunotoxins that target specific macrophage surface markers (e.g., CD64) could selectively eliminate activated, pro-inflammatory macrophages.
• Inhibiting Macrophage Activation and Function: Targeting key intracellular inflammatory signaling pathways, such as the JAK-STAT, NF-κB, and MAPK pathways. Bruton's tyrosine kinase (BTK) is important for Fc receptor signaling and macrophage activation. BTK inhibitors can directly suppress macrophage function in addition to their effects on B cells.
• Macrophage Reprogramming: This is one of the most promising and advanced strategies, aiming to convert pathogenic M1 macrophages into reparative M2 macrophages.
• Drug-Loaded Nanoparticles: Designing nanocarriers that can specifically deliver drugs (e.g., corticosteroids, STAT6 agonists) to macrophages to induce their polarization towards an M2 phenotype.

Creative Biolabs' Macrophage Research Solutions

To support the global research community in the field of autoimmunity, Creative Biolabs has developed a comprehensive and highly customizable suite of macrophage research services. Our platform combines state-of-the-art technologies with a team of senior immunologists to provide you with reliable, reproducible data.

Creative Biolabs is committed to being your most trusted partner, empowering your breakthroughs with our leading-edge technologies and services.

• Highly customizable: We work closely with our clients to design and optimize experimental protocols tailored to your specific research needs.
• High-quality cell sources: All primary cells undergo rigorous quality control to ensure high purity and viability.
• Multi-dimensional detection platforms: We provide a one-stop shop for comprehensive analysis, from genes and proteins to cellular functions.
• Experienced expert team: Our scientists will provide you with professional technical support and in-depth data interpretation.

Related Products

Curated, assay-validated reagents and tools that plug directly into our autoimmune macrophage workflows. For Research Use Only.

Scientific Resources

Q & A

Q: Can I combine multiple disease modules in one study?

A: Yes. Many sponsors run a core macrophage panel across two or more modules (e.g., RA and SLE) to compare signatures side-by-side. We coordinate donors, controls, and timepoints to keep datasets comparable and statistically sound.

Q: What if my compound's primary target is outside macrophages?

A: That is common. We use co-cultures and conditioned media to read macrophage-mediated consequences of upstream events (e.g., T-cell or keratinocyte signals), revealing indirect but critical macrophage contributions to efficacy or liability.

Q: Can you evaluate nanoparticle or targeted delivery systems?

A: Absolutely. We profile uptake, intracellular routing, endosomal escape proxies, cytokine induction, and functional endpoints. We also test targeting ligands under inflammatory vs. resolution states to capture state-dependent uptake.

Q: What is the typical timeline for a macrophage-based autoimmune study?

A: The timeline includes the time needed for model establishment, cell polarization, testing of test articles, and readout analysis. We provide you with regular updates throughout the study, including preliminary data if requested, so you can make timely decisions regarding your research. If you require accelerated timelines, we can discuss expedited options based on project scope and resource availability.

Discuss your autoimmune indication, mechanism hypotheses, and decision timeline with our scientists. Contact Creative Biolabs to design a study that moves your program forward with data you can trust. All services are for research use only and not for clinical applications.

References

1. Ma, Wen-Tao, et al. "The role of monocytes and macrophages in autoimmune diseases: a comprehensive review." Frontiers in immunology 10 (2019): 1140. https://doi.org/10.3389/fimmu.2019.01140
2. Distributed under Open Access license CC BY 4.0, without modification.