TY - JOUR
T1 - Autophagy drives plasticity and functional polarization of tumor-associated macrophages
AU - Kuo, Wan Ting
AU - Chang, Jia Ming
AU - Chen, Chien Chin
AU - Tsao, Nina
AU - Chang, Chih Peng
N1 - Funding Information:
This work was supported by Ministry of Science and Technology, Taiwan (Grant Nos. MOST 107‐2320‐B‐006‐026‐MY3, MOST 107‐2321‐B‐006‐020, and MOST 110‐2622‐B‐006‐006‐CC1). All figures were created with BioRender.com .
Funding Information:
Ministry of Science and Technology, Taiwan, Grant/Award Numbers: MOST 107‐2320‐B‐006‐026‐MY3, MOST 107‐2321‐B‐006‐020, MOST 110‐2622‐B‐006‐006‐CC1 Funding information
Publisher Copyright:
© 2021 International Union of Biochemistry and Molecular Biology.
PY - 2022/2
Y1 - 2022/2
N2 - Tumor-associated macrophages (TAMs) are a major component of the tumor microenvironment (TME) and are key cells in regulating tumor development, metastasis, immune responses, inflammation, and chemoresistance. In response to TME stimulation, circulating monocytes are recruited and differentiated as TAMs. Most TAMs are defined as alternatively activated (M2) phenotype to create immunosuppressive TME and support tumor progression. In contrast, classically activated (M1) TAMs can produce pro-inflammatory cytokines and enhance immune responses against tumor development. Autophagy is a conserved catabolic process to control cellular homeostasis and biological function. Emerging evidence reveals crucial contribution of autophagy in modulating TAM plasticity and functional polarization in TME. In this review, we introduce the current understanding of autophagy-regulated TAM function in development of cancer. We focus on how autophagy modulates antigen presentation, LC3-associated phagocytosis, cytokine secretion, inflammasome regulation, recruitment, differentiation, and polarization of TAMs and suggest strategies for potential therapeutics by targeting autophagy in TAMs. We expect this review can provide a new notion of future cancer immunotherapy.
AB - Tumor-associated macrophages (TAMs) are a major component of the tumor microenvironment (TME) and are key cells in regulating tumor development, metastasis, immune responses, inflammation, and chemoresistance. In response to TME stimulation, circulating monocytes are recruited and differentiated as TAMs. Most TAMs are defined as alternatively activated (M2) phenotype to create immunosuppressive TME and support tumor progression. In contrast, classically activated (M1) TAMs can produce pro-inflammatory cytokines and enhance immune responses against tumor development. Autophagy is a conserved catabolic process to control cellular homeostasis and biological function. Emerging evidence reveals crucial contribution of autophagy in modulating TAM plasticity and functional polarization in TME. In this review, we introduce the current understanding of autophagy-regulated TAM function in development of cancer. We focus on how autophagy modulates antigen presentation, LC3-associated phagocytosis, cytokine secretion, inflammasome regulation, recruitment, differentiation, and polarization of TAMs and suggest strategies for potential therapeutics by targeting autophagy in TAMs. We expect this review can provide a new notion of future cancer immunotherapy.
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U2 - 10.1002/iub.2543
DO - 10.1002/iub.2543
M3 - Article
C2 - 34467634
AN - SCOPUS:85113950225
SN - 1521-6543
VL - 74
SP - 157
EP - 169
JO - IUBMB Life
JF - IUBMB Life
IS - 2
ER -