Tumor-derived exosomes induce PD1+ macrophage population in human gastric cancer that promotes disease progression

Macrophages constitute a major component of tumor-infiltrating immune cells. M2 macrophages have been reported to promote tumor progression through promoting tumor angiogenesis and metastasis and regulating T-cell function. Here, we identified a protumorigenic subset of macrophages that constitutive...

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Vydáno v:Oncogenesis (New York, NY) Ročník 7; číslo 5; s. 41 - 11
Hlavní autoři: Wang, Furong, Li, Bin, Wei, Yucai, Zhao, Yang, Wang, Li, Zhang, Peng, Yang, Jinwei, He, Wenting, Chen, Hao, Jiao, Zuoyi, Li, Yumin
Médium: Journal Article
Jazyk:angličtina
Vydáno: London Nature Publishing Group UK 25.05.2018
Nature Publishing Group
Témata:
13/31
38/77
631/250/251
631/67/1059/2325
Angiogenesis
Apoptosis
CD8 antigen
Cell Biology
Cell death
Chemokines
Exosomes
Gastric cancer
Human Genetics
Immune response
Immunosuppressive agents
Immunotherapy
Interleukin 10
Interleukin 12
Internal Medicine
Lymphocytes T
Macrophages
Major histocompatibility complex
Medicine
Medicine & Public Health
Metastases
Monocytes
Oncology
Ovalbumin
PD-1 protein
Phenotypes
Recovery of function
T cell receptors
Tumor-infiltrating lymphocytes
ISSN:2157-9024, 2157-9024
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Abstract Macrophages constitute a major component of tumor-infiltrating immune cells. M2 macrophages have been reported to promote tumor progression through promoting tumor angiogenesis and metastasis and regulating T-cell function. Here, we identified a protumorigenic subset of macrophages that constitutively expressed programmed cell death 1 (PD1) and accumulated in advanced-stage gastric cancer (GC). These PD1 + tumor-associated macrophages (TAMs) exhibited an M2-like surface profile, with a significant increase in the expression of CD206, IL-10, and CCL1, and a clear decrease in the expression of MHC class II, CD64, and IL-12 and the ability to phagocytose ovalbumin. Moreover, PD1 + TAMs can suppress CD8 + T-cell function and this immunosuppressive activity can effectively be enhanced upon triggering PD1 signal. GC-derived exosomes effectively educated monocytes to differentiate into PD1 + TAMs with M2 phenotypic and functional characteristics. Together, our results are the first to show that GC-derived exosomes can effectively induce PD1 + TAM generation, and these cells can produce a large number of IL-10, impair CD8 + T-cell function, and thereby create conditions that promote GC progression. Thus, methods in which immunotherapy is combined with targeting PD1 + TAMs and tumor-derived exosomes should be used to restore immune function in GC patients.
AbstractList Macrophages constitute a major component of tumor-infiltrating immune cells. M2 macrophages have been reported to promote tumor progression through promoting tumor angiogenesis and metastasis and regulating T-cell function. Here, we identified a protumorigenic subset of macrophages that constitutively expressed programmed cell death 1 (PD1) and accumulated in advanced-stage gastric cancer (GC). These PD1 + tumor-associated macrophages (TAMs) exhibited an M2-like surface profile, with a significant increase in the expression of CD206, IL-10, and CCL1, and a clear decrease in the expression of MHC class II, CD64, and IL-12 and the ability to phagocytose ovalbumin. Moreover, PD1 + TAMs can suppress CD8 + T-cell function and this immunosuppressive activity can effectively be enhanced upon triggering PD1 signal. GC-derived exosomes effectively educated monocytes to differentiate into PD1 + TAMs with M2 phenotypic and functional characteristics. Together, our results are the first to show that GC-derived exosomes can effectively induce PD1 + TAM generation, and these cells can produce a large number of IL-10, impair CD8 + T-cell function, and thereby create conditions that promote GC progression. Thus, methods in which immunotherapy is combined with targeting PD1 + TAMs and tumor-derived exosomes should be used to restore immune function in GC patients.
AbstractMacrophages constitute a major component of tumor-infiltrating immune cells. M2 macrophages have been reported to promote tumor progression through promoting tumor angiogenesis and metastasis and regulating T-cell function. Here, we identified a protumorigenic subset of macrophages that constitutively expressed programmed cell death 1 (PD1) and accumulated in advanced-stage gastric cancer (GC). These PD1+ tumor-associated macrophages (TAMs) exhibited an M2-like surface profile, with a significant increase in the expression of CD206, IL-10, and CCL1, and a clear decrease in the expression of MHC class II, CD64, and IL-12 and the ability to phagocytose ovalbumin. Moreover, PD1+ TAMs can suppress CD8+ T-cell function and this immunosuppressive activity can effectively be enhanced upon triggering PD1 signal. GC-derived exosomes effectively educated monocytes to differentiate into PD1+ TAMs with M2 phenotypic and functional characteristics. Together, our results are the first to show that GC-derived exosomes can effectively induce PD1+ TAM generation, and these cells can produce a large number of IL-10, impair CD8+ T-cell function, and thereby create conditions that promote GC progression. Thus, methods in which immunotherapy is combined with targeting PD1+ TAMs and tumor-derived exosomes should be used to restore immune function in GC patients.
Macrophages constitute a major component of tumor-infiltrating immune cells. M2 macrophages have been reported to promote tumor progression through promoting tumor angiogenesis and metastasis and regulating T-cell function. Here, we identified a protumorigenic subset of macrophages that constitutively expressed programmed cell death 1 (PD1) and accumulated in advanced-stage gastric cancer (GC). These PD1+ tumor-associated macrophages (TAMs) exhibited an M2-like surface profile, with a significant increase in the expression of CD206, IL-10, and CCL1, and a clear decrease in the expression of MHC class II, CD64, and IL-12 and the ability to phagocytose ovalbumin. Moreover, PD1+ TAMs can suppress CD8+ T-cell function and this immunosuppressive activity can effectively be enhanced upon triggering PD1 signal. GC-derived exosomes effectively educated monocytes to differentiate into PD1+ TAMs with M2 phenotypic and functional characteristics. Together, our results are the first to show that GC-derived exosomes can effectively induce PD1+ TAM generation, and these cells can produce a large number of IL-10, impair CD8+ T-cell function, and thereby create conditions that promote GC progression. Thus, methods in which immunotherapy is combined with targeting PD1+ TAMs and tumor-derived exosomes should be used to restore immune function in GC patients.
Macrophages constitute a major component of tumor-infiltrating immune cells. M2 macrophages have been reported to promote tumor progression through promoting tumor angiogenesis and metastasis and regulating T-cell function. Here, we identified a protumorigenic subset of macrophages that constitutively expressed programmed cell death 1 (PD1) and accumulated in advanced-stage gastric cancer (GC). These PD1+ tumor-associated macrophages (TAMs) exhibited an M2-like surface profile, with a significant increase in the expression of CD206, IL-10, and CCL1, and a clear decrease in the expression of MHC class II, CD64, and IL-12 and the ability to phagocytose ovalbumin. Moreover, PD1+ TAMs can suppress CD8+ T-cell function and this immunosuppressive activity can effectively be enhanced upon triggering PD1 signal. GC-derived exosomes effectively educated monocytes to differentiate into PD1+ TAMs with M2 phenotypic and functional characteristics. Together, our results are the first to show that GC-derived exosomes can effectively induce PD1+ TAM generation, and these cells can produce a large number of IL-10, impair CD8+ T-cell function, and thereby create conditions that promote GC progression. Thus, methods in which immunotherapy is combined with targeting PD1+ TAMs and tumor-derived exosomes should be used to restore immune function in GC patients.Macrophages constitute a major component of tumor-infiltrating immune cells. M2 macrophages have been reported to promote tumor progression through promoting tumor angiogenesis and metastasis and regulating T-cell function. Here, we identified a protumorigenic subset of macrophages that constitutively expressed programmed cell death 1 (PD1) and accumulated in advanced-stage gastric cancer (GC). These PD1+ tumor-associated macrophages (TAMs) exhibited an M2-like surface profile, with a significant increase in the expression of CD206, IL-10, and CCL1, and a clear decrease in the expression of MHC class II, CD64, and IL-12 and the ability to phagocytose ovalbumin. Moreover, PD1+ TAMs can suppress CD8+ T-cell function and this immunosuppressive activity can effectively be enhanced upon triggering PD1 signal. GC-derived exosomes effectively educated monocytes to differentiate into PD1+ TAMs with M2 phenotypic and functional characteristics. Together, our results are the first to show that GC-derived exosomes can effectively induce PD1+ TAM generation, and these cells can produce a large number of IL-10, impair CD8+ T-cell function, and thereby create conditions that promote GC progression. Thus, methods in which immunotherapy is combined with targeting PD1+ TAMs and tumor-derived exosomes should be used to restore immune function in GC patients.
Macrophages constitute a major component of tumor-infiltrating immune cells. M2 macrophages have been reported to promote tumor progression through promoting tumor angiogenesis and metastasis and regulating T-cell function. Here, we identified a protumorigenic subset of macrophages that constitutively expressed programmed cell death 1 (PD1) and accumulated in advanced-stage gastric cancer (GC). These PD1 tumor-associated macrophages (TAMs) exhibited an M2-like surface profile, with a significant increase in the expression of CD206, IL-10, and CCL1, and a clear decrease in the expression of MHC class II, CD64, and IL-12 and the ability to phagocytose ovalbumin. Moreover, PD1 TAMs can suppress CD8 T-cell function and this immunosuppressive activity can effectively be enhanced upon triggering PD1 signal. GC-derived exosomes effectively educated monocytes to differentiate into PD1 TAMs with M2 phenotypic and functional characteristics. Together, our results are the first to show that GC-derived exosomes can effectively induce PD1 TAM generation, and these cells can produce a large number of IL-10, impair CD8 T-cell function, and thereby create conditions that promote GC progression. Thus, methods in which immunotherapy is combined with targeting PD1 TAMs and tumor-derived exosomes should be used to restore immune function in GC patients.
ArticleNumber 41
Author Jiao, Zuoyi
Zhang, Peng
Wang, Li
Li, Yumin
Li, Bin
Zhao, Yang
Wei, Yucai
He, Wenting
Chen, Hao
Wang, Furong
Yang, Jinwei
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  surname: Li
  fullname: Li, Bin
  organization: Department of Thoracic Surgery, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College
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  givenname: Yucai
  surname: Wei
  fullname: Wei, Yucai
  organization: School of Basic Medical Science, Lanzhou University, Department of General Surgery, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College
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  givenname: Yang
  surname: Zhao
  fullname: Zhao, Yang
  organization: Gansu Provincial Key Laboratory of Digestive System Tumors, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College
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  fullname: Zhang, Peng
  organization: Department of Pathology, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College, Gansu Provincial Key Laboratory of Digestive System Tumors, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College
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  organization: Gansu Provincial Key Laboratory of Digestive System Tumors, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College
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  organization: Gansu Provincial Key Laboratory of Digestive System Tumors, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College
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  givenname: Hao
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  organization: Gansu Provincial Key Laboratory of Digestive System Tumors, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College, Department of General Surgery, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College
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  organization: Gansu Provincial Key Laboratory of Digestive System Tumors, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College, School of Life Sciences, Lanzhou University, Department of General Surgery, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29799520$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright The Author(s) 2018
2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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– reference: 35136026 - Oncogenesis. 2022 Feb 8;11(1):7
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Snippet Macrophages constitute a major component of tumor-infiltrating immune cells. M2 macrophages have been reported to promote tumor progression through promoting...
AbstractMacrophages constitute a major component of tumor-infiltrating immune cells. M2 macrophages have been reported to promote tumor progression through...
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StartPage 41
SubjectTerms 13/31
38/77
631/250/251
631/67/1059/2325
Angiogenesis
Apoptosis
CD8 antigen
Cell Biology
Cell death
Chemokines
Exosomes
Gastric cancer
Human Genetics
Immune response
Immunosuppressive agents
Immunotherapy
Interleukin 10
Interleukin 12
Internal Medicine
Lymphocytes T
Macrophages
Major histocompatibility complex
Medicine
Medicine & Public Health
Metastases
Monocytes
Oncology
Ovalbumin
PD-1 protein
Phenotypes
Recovery of function
T cell receptors
Tumor-infiltrating lymphocytes
Title Tumor-derived exosomes induce PD1+ macrophage population in human gastric cancer that promotes disease progression
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