Macrophage Reprogramming Service

By applying our state-of-the-art Macrophage Therapeutics Development Platform as well as industry-leading expertise, Creative Biolabs provides overall solutions for macrophage reprogramming, focusing on innovative research. Our multidisciplinary scientists will work together closely to address the scientific and technical challenges in macrophage reprogramming.

Introduction to Macrophage Polarization

Responding to different microenvironments, primary macrophages (M0) can be polarized toward pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes. M1 polarization is induced by bacterial lipopolysaccharides (LPS) or the pro-inflammatory cytokine interferon-gamma (IFN-γ), and is therefore generally associated with the pathogenesis of various inflammatory diseases. While M2 are induced by anti-inflammatory cytokines, interleukin (IL)-10, IL-4 or IL-13 and are typically associated with the immune response to parasites, wound healing and promotion of angiogenesis. M1 macrophages produce numerous proinflammatory mediators, such as tumor necrosis factor α (TNFα), IL12 and IL23, nitric oxide (NO), and other reactive oxygen species (ROS), which are important for host defense against pathogens. By contrast, M2 macrophages secrete significant amounts of IL-10 and polyamines, adapting immune responses to promote angiogenesis and tissue remodeling. At the transcriptional level, M1 and M2 macrophages are regulated through different mechanisms. M2 macrophages favor tumor growth. In cancer disease, tumor-associated macrophages (TAMs) usually exhibit an M2 phenotype and participate in tumor angiogenesis, tumor invasion and metastasis, immunosuppression, and cell activation. Reprogramming of TAMs toward M1-like macrophages would thus be an efficient way to promote tumor regression.

Fig.1 Scheme of current strategies for TAM reprogramming. (Fiani, Maria Luisa, et al., 2020)Fig.1 Scheme of current strategies for TAM reprogramming.1,2

Macrophage Reprogramming Service at Creative Biolabs

In response to different microenvironments, such as microbial signals, tissue damage, cytokines and metabolic products, macrophages from healthy tissues can undergo reprogramming. Creative Biolabs has organized a staff of outstanding scientists who have engaged in the research of macrophage reprogramming for many years. Our seasoned scientists have developed several efficient strategies for macrophage reprogramming, including Reprogramming Macrophages Employing Gene Regulatory Networks, Reprogramming Macrophages By Nanoparticles, Reprogramming Macrophages by microRNA and In Vivo Lentivirus-based Macrophage Reprogramming Services.

TAMs play a central role in tumor progression, metastasis, and recurrence after treatment. The pro-tumoral functions of TAMs and their ability to be reprogrammed from M2-like macrophages toward M1 phenotype, make them an attractive target for anticancer therapies. Scientists at Creative Biolabs have developed several approaches to modulate TAM, including TAM Depletion, Inhibition of Circulating Monocyte Recruitment into The Tumor, Blockade of M2 Phenotype and Reprogramming TAM Toward M1-like Macrophage to modulate TAMs. Moreover, we have constructed a large small molecular compound library for High-Throughput Phenotypic Screening of New Compounds for macrophage reprogramming, and we provide the most comprehensive transcriptional analysis for the Identification of Targets for M1-activating compounds and M2-activating compounds.

Professional scientists, a comprehensive powerful platform, and abundant experience make Creative Biolabs a perfect partner to help our clients in macrophage reprogramming. For more detailed information, please feel free to contact us or send us your inquiry or question.

References

  1. Fiani, Maria Luisa, et al. "Exploiting manipulated small extracellular vesicles to subvert immunosuppression at the tumor microenvironment through mannose receptor/CD206 targeting." International Journal of Molecular Sciences 21.17 (2020): 6318.
  2. Under Open Access license CC BY 4.0, without modification.
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