Hybrid Cellular Nanovesicles Block PD‐L1 Signal and Repolarize M2 Macrophages for Cancer Immunotherapy

The PD1/PD‐L1 immune checkpoint blocking is a promising therapy, while immunosuppressive tumor microenvironment (TME) and poor tumor penetration of therapeutic antibodies limit its efficacy. Repolarization of tumor‐associated macrophages (TAMs) offers a potential method to ameliorate immunosuppressi...

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Published inSmall (Weinheim an der Bergstrasse, Germany) Vol. 20; no. 31; pp. e2311702 - n/a
Main Authors Zhao, Chenchen, Pan, Yuanwei, Liu, Lujie, Zhang, Jing, Wu, Xianjia, Liu, Yu, Zhao, Xing‐Zhong, Rao, Lang
Format Journal Article
LanguageEnglish
Published Germany Wiley Subscription Services, Inc 01.08.2024
Subjects
Animals
B7-H1 Antigen - metabolism
biomimetic nanoparticles
Blocking
Cancer
cancer immunotherapy
Cell Line, Tumor
cell membrane vesicles
Cell membranes
Effectiveness
Female
Humans
immune checkpoint blockade
Immunosuppression
Immunotherapy
Immunotherapy - methods
Lymphocytes
macrophage polarization
Macrophages
Macrophages - metabolism
Mice
Nanoparticles - chemistry
Neoplasms - immunology
Neoplasms - pathology
Neoplasms - therapy
Programmed Cell Death 1 Receptor - metabolism
Signal Transduction
Tumor Microenvironment
biomimetic nanoparticles
macrophage polarization
cell membrane vesicles
cancer immunotherapy
immune checkpoint blockade
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Abstract The PD1/PD‐L1 immune checkpoint blocking is a promising therapy, while immunosuppressive tumor microenvironment (TME) and poor tumor penetration of therapeutic antibodies limit its efficacy. Repolarization of tumor‐associated macrophages (TAMs) offers a potential method to ameliorate immunosuppression of TME and further boost T cell antitumor immunity. Herein, hybrid cell membrane biomimetic nanovesicles (hNVs) are developed by fusing M1 macrophage‐derived nanovesicles (M1‐NVs) and PD1‐overexpressed tumor cell‐derived nanovesicles (PD1‐NVs) to improve cancer immunotherapy. The M1‐NVs promote the transformation of M2‐like TAMs to M1‐like phenotype and further increase the release of pro‐inflammatory cytokines, resulting in improved immunosuppressive TME. Concurrently, the PD1‐NVs block PD1/PD‐L1 pathway, which boosts cancer immunotherapy when combined with M1‐NVs. In a breast cancer mouse model, the hNVs efficiently accumulate at the tumor site after intravenous injection and significantly inhibit the tumor growth. Mechanically, the M1 macrophages and CD8+ T lymphocytes in TME increase by twofold after the treatment, indicating effective immune activation. These results suggest the hNVs as a promising strategy to integrate TME improvement with PD1/PD‐L1 blockade for cancer immunotherapy. Hybrid cellular nanovesicles (hNVs) are prepared by fusing M1 macrophage‐derived nanovesicles (M1‐NVs) and PD1‐overexpressed tumor cell‐derived nanovesicles (PD1‐NVs) for enhanced cancer immunotherapy. The M1‐NVs promote the repolarization of M2‐like TAMs to M1‐like phenotype and further increase the release of pro‐inflammatory cytokines, resulting in improved immunosuppressive tumor microenvironment. Concurrently, the PD1‐NVs block PD1/PD‐L1 pathway, synergizing with M1‐NVs to boost cancer immunotherapy.
AbstractList The PD1/PD‐L1 immune checkpoint blocking is a promising therapy, while immunosuppressive tumor microenvironment (TME) and poor tumor penetration of therapeutic antibodies limit its efficacy. Repolarization of tumor‐associated macrophages (TAMs) offers a potential method to ameliorate immunosuppression of TME and further boost T cell antitumor immunity. Herein, hybrid cell membrane biomimetic nanovesicles (hNVs) are developed by fusing M1 macrophage‐derived nanovesicles (M1‐NVs) and PD1‐overexpressed tumor cell‐derived nanovesicles (PD1‐NVs) to improve cancer immunotherapy. The M1‐NVs promote the transformation of M2‐like TAMs to M1‐like phenotype and further increase the release of pro‐inflammatory cytokines, resulting in improved immunosuppressive TME. Concurrently, the PD1‐NVs block PD1/PD‐L1 pathway, which boosts cancer immunotherapy when combined with M1‐NVs. In a breast cancer mouse model, the hNVs efficiently accumulate at the tumor site after intravenous injection and significantly inhibit the tumor growth. Mechanically, the M1 macrophages and CD8+ T lymphocytes in TME increase by twofold after the treatment, indicating effective immune activation. These results suggest the hNVs as a promising strategy to integrate TME improvement with PD1/PD‐L1 blockade for cancer immunotherapy. Hybrid cellular nanovesicles (hNVs) are prepared by fusing M1 macrophage‐derived nanovesicles (M1‐NVs) and PD1‐overexpressed tumor cell‐derived nanovesicles (PD1‐NVs) for enhanced cancer immunotherapy. The M1‐NVs promote the repolarization of M2‐like TAMs to M1‐like phenotype and further increase the release of pro‐inflammatory cytokines, resulting in improved immunosuppressive tumor microenvironment. Concurrently, the PD1‐NVs block PD1/PD‐L1 pathway, synergizing with M1‐NVs to boost cancer immunotherapy.
The PD1/PD-L1 immune checkpoint blocking is a promising therapy, while immunosuppressive tumor microenvironment (TME) and poor tumor penetration of therapeutic antibodies limit its efficacy. Repolarization of tumor-associated macrophages (TAMs) offers a potential method to ameliorate immunosuppression of TME and further boost T cell antitumor immunity. Herein, hybrid cell membrane biomimetic nanovesicles (hNVs) are developed by fusing M1 macrophage-derived nanovesicles (M1-NVs) and PD1-overexpressed tumor cell-derived nanovesicles (PD1-NVs) to improve cancer immunotherapy. The M1-NVs promote the transformation of M2-like TAMs to M1-like phenotype and further increase the release of pro-inflammatory cytokines, resulting in improved immunosuppressive TME. Concurrently, the PD1-NVs block PD1/PD-L1 pathway, which boosts cancer immunotherapy when combined with M1-NVs. In a breast cancer mouse model, the hNVs efficiently accumulate at the tumor site after intravenous injection and significantly inhibit the tumor growth. Mechanically, the M1 macrophages and CD8 T lymphocytes in TME increase by twofold after the treatment, indicating effective immune activation. These results suggest the hNVs as a promising strategy to integrate TME improvement with PD1/PD-L1 blockade for cancer immunotherapy.
The PD1/PD‐L1 immune checkpoint blocking is a promising therapy, while immunosuppressive tumor microenvironment (TME) and poor tumor penetration of therapeutic antibodies limit its efficacy. Repolarization of tumor‐associated macrophages (TAMs) offers a potential method to ameliorate immunosuppression of TME and further boost T cell antitumor immunity. Herein, hybrid cell membrane biomimetic nanovesicles (hNVs) are developed by fusing M1 macrophage‐derived nanovesicles (M1‐NVs) and PD1‐overexpressed tumor cell‐derived nanovesicles (PD1‐NVs) to improve cancer immunotherapy. The M1‐NVs promote the transformation of M2‐like TAMs to M1‐like phenotype and further increase the release of pro‐inflammatory cytokines, resulting in improved immunosuppressive TME. Concurrently, the PD1‐NVs block PD1/PD‐L1 pathway, which boosts cancer immunotherapy when combined with M1‐NVs. In a breast cancer mouse model, the hNVs efficiently accumulate at the tumor site after intravenous injection and significantly inhibit the tumor growth. Mechanically, the M1 macrophages and CD8+ T lymphocytes in TME increase by twofold after the treatment, indicating effective immune activation. These results suggest the hNVs as a promising strategy to integrate TME improvement with PD1/PD‐L1 blockade for cancer immunotherapy.
The PD1/PD-L1 immune checkpoint blocking is a promising therapy, while immunosuppressive tumor microenvironment (TME) and poor tumor penetration of therapeutic antibodies limit its efficacy. Repolarization of tumor-associated macrophages (TAMs) offers a potential method to ameliorate immunosuppression of TME and further boost T cell antitumor immunity. Herein, hybrid cell membrane biomimetic nanovesicles (hNVs) are developed by fusing M1 macrophage-derived nanovesicles (M1-NVs) and PD1-overexpressed tumor cell-derived nanovesicles (PD1-NVs) to improve cancer immunotherapy. The M1-NVs promote the transformation of M2-like TAMs to M1-like phenotype and further increase the release of pro-inflammatory cytokines, resulting in improved immunosuppressive TME. Concurrently, the PD1-NVs block PD1/PD-L1 pathway, which boosts cancer immunotherapy when combined with M1-NVs. In a breast cancer mouse model, the hNVs efficiently accumulate at the tumor site after intravenous injection and significantly inhibit the tumor growth. Mechanically, the M1 macrophages and CD8+ T lymphocytes in TME increase by twofold after the treatment, indicating effective immune activation. These results suggest the hNVs as a promising strategy to integrate TME improvement with PD1/PD-L1 blockade for cancer immunotherapy.The PD1/PD-L1 immune checkpoint blocking is a promising therapy, while immunosuppressive tumor microenvironment (TME) and poor tumor penetration of therapeutic antibodies limit its efficacy. Repolarization of tumor-associated macrophages (TAMs) offers a potential method to ameliorate immunosuppression of TME and further boost T cell antitumor immunity. Herein, hybrid cell membrane biomimetic nanovesicles (hNVs) are developed by fusing M1 macrophage-derived nanovesicles (M1-NVs) and PD1-overexpressed tumor cell-derived nanovesicles (PD1-NVs) to improve cancer immunotherapy. The M1-NVs promote the transformation of M2-like TAMs to M1-like phenotype and further increase the release of pro-inflammatory cytokines, resulting in improved immunosuppressive TME. Concurrently, the PD1-NVs block PD1/PD-L1 pathway, which boosts cancer immunotherapy when combined with M1-NVs. In a breast cancer mouse model, the hNVs efficiently accumulate at the tumor site after intravenous injection and significantly inhibit the tumor growth. Mechanically, the M1 macrophages and CD8+ T lymphocytes in TME increase by twofold after the treatment, indicating effective immune activation. These results suggest the hNVs as a promising strategy to integrate TME improvement with PD1/PD-L1 blockade for cancer immunotherapy.
The PD1/PD‐L1 immune checkpoint blocking is a promising therapy, while immunosuppressive tumor microenvironment (TME) and poor tumor penetration of therapeutic antibodies limit its efficacy. Repolarization of tumor‐associated macrophages (TAMs) offers a potential method to ameliorate immunosuppression of TME and further boost T cell antitumor immunity. Herein, hybrid cell membrane biomimetic nanovesicles (hNVs) are developed by fusing M1 macrophage‐derived nanovesicles (M1‐NVs) and PD1‐overexpressed tumor cell‐derived nanovesicles (PD1‐NVs) to improve cancer immunotherapy. The M1‐NVs promote the transformation of M2‐like TAMs to M1‐like phenotype and further increase the release of pro‐inflammatory cytokines, resulting in improved immunosuppressive TME. Concurrently, the PD1‐NVs block PD1/PD‐L1 pathway, which boosts cancer immunotherapy when combined with M1‐NVs. In a breast cancer mouse model, the hNVs efficiently accumulate at the tumor site after intravenous injection and significantly inhibit the tumor growth. Mechanically, the M1 macrophages and CD8 + T lymphocytes in TME increase by twofold after the treatment, indicating effective immune activation. These results suggest the hNVs as a promising strategy to integrate TME improvement with PD1/PD‐L1 blockade for cancer immunotherapy.
Author Zhang, Jing
Liu, Yu
Zhao, Xing‐Zhong
Zhao, Chenchen
Liu, Lujie
Pan, Yuanwei
Wu, Xianjia
Rao, Lang
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Keywords biomimetic nanoparticles
macrophage polarization
cell membrane vesicles
cancer immunotherapy
immune checkpoint blockade
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Snippet The PD1/PD‐L1 immune checkpoint blocking is a promising therapy, while immunosuppressive tumor microenvironment (TME) and poor tumor penetration of therapeutic...
The PD1/PD-L1 immune checkpoint blocking is a promising therapy, while immunosuppressive tumor microenvironment (TME) and poor tumor penetration of therapeutic...
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SubjectTerms Animals
B7-H1 Antigen - metabolism
biomimetic nanoparticles
Blocking
Cancer
cancer immunotherapy
Cell Line, Tumor
cell membrane vesicles
Cell membranes
Effectiveness
Female
Humans
immune checkpoint blockade
Immunosuppression
Immunotherapy
Immunotherapy - methods
Lymphocytes
macrophage polarization
Macrophages
Macrophages - metabolism
Mice
Nanoparticles - chemistry
Neoplasms - immunology
Neoplasms - pathology
Neoplasms - therapy
Programmed Cell Death 1 Receptor - metabolism
Signal Transduction
Tumor Microenvironment
Title Hybrid Cellular Nanovesicles Block PD‐L1 Signal and Repolarize M2 Macrophages for Cancer Immunotherapy
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fsmll.202311702
https://www.ncbi.nlm.nih.gov/pubmed/38456371
https://www.proquest.com/docview/3086818598
https://www.proquest.com/docview/2954776468
Volume 20
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