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Published on: August 2, 2021
One-Dimensional Rod-like Tobacco Mosaic Virus Promotes Macrophage Polarization for a Tumor-Suppressive
Jinzhao Ou1,2, Meng Zhu1, Xiaoyan Ju1
1Key Laboratory of Photochemical Conversion and Optoelectronic Materials, Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, 29 Zhongguancun East Road, Beijing 100190, P.R. China.
Abstract:
The phenotype of tumor-associated macrophages plays an important role in their function of regulating the tumor immune microenvironment. The M1-phenotype macrophages display tumor-killing and immune activating functions. Here we show that the tobacco mosaic virus (TMV), a rod-like plant virus, can polarize macrophages to an M1 phenotype and shape a tumor-suppressive microenvironment. RAW 264.7 cells and bone marrow derived-macrophages (BMDMs) can recognize TMV via Toll-like receptor-4, and then the MAPK and NF-κB signaling pathways are activated, leading to the production of pro-inflammatory factors. Furthermore, the in vivo assessments on a subcutaneous co-injection tumor model show that the TMV-polarized BMDMs shape a tumor-suppressive microenvironment, resulting in remarkable delay of 4T1 tumor growth. Another in vivo assessment on an established tumor model indicates the high tumor-metastasis-inhibiting capacity of TMV-polarized BMDMs. This work suggests a role for this plant virus in macrophage-mediated therapeutic approaches and provides a strategy for tumor immunotherapy.
Insights
Tobacco mosaic virus (TMV) programs macrophages to an M1 phenotype, creating a tumor-suppressive environment. This plant virus demonstrates potential for cancer immunotherapy by inhibiting tumor growth and metastasis.
Area of Science:
- Immunology
- Virology
- Oncology
Background:
- Tumor-associated macrophages (TAMs) critically regulate the tumor immune microenvironment.
- M1-phenotype macrophages exhibit potent anti-tumor and immune-stimulating activities.
- Targeting macrophage polarization offers a promising avenue for cancer immunotherapy.
Purpose of the Study:
- To investigate the potential of tobacco mosaic virus (TMV) in polarizing macrophages towards an M1 phenotype.
- To evaluate the efficacy of TMV-induced macrophage polarization in shaping a tumor-suppressive microenvironment.
- To assess the therapeutic potential of TMV-polarized macrophages in inhibiting tumor growth and metastasis.
Main Methods:
- RAW 264.7 cells and bone marrow-derived macrophages (BMDMs) were stimulated with TMV.
- Macrophage recognition of TMV was assessed via Toll-like receptor-4 (TLR4) signaling.
- MAPK and NF-κB pathways activation and pro-inflammatory cytokine production were analyzed.
- In vivo studies utilized subcutaneous co-injection and established tumor models in mice.
Main Results:
- TMV was recognized by macrophages through TLR4, activating MAPK and NF-κB signaling pathways.
- TMV induced the production of pro-inflammatory factors, polarizing macrophages to an M1 phenotype.
- TMV-polarized BMDMs significantly delayed 4T1 tumor growth in a subcutaneous co-injection model.
- TMV-polarized BMDMs demonstrated substantial inhibition of tumor metastasis in an established tumor model.
Conclusions:
- TMV effectively polarizes macrophages to an M1 phenotype via TLR4-mediated signaling.
- TMV-induced M1 macrophages create a tumor-suppressive microenvironment, inhibiting tumor growth and metastasis.
- TMV presents a novel plant virus-based strategy for macrophage-mediated cancer immunotherapy.
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