| Tong Zhu,Guihua Wang. The interaction between end-metabolites and immune escape. Oncol Transl Med, 2022, 8: 57-73. |
| The interaction between end-metabolites and immune escape |
| The interaction between end-metabolites and immune escape |
| Received:April 26, 2022 Revised:April 26, 2022 |
| DOI:10.1007/s10330-022-0573-3 |
| 中文关键词: lactate acid; adenosine; reactive oxygen species; tumour; immune escape |
| 英文关键词: lactate acid; adenosine; reactive oxygen species; tumour; immune escape |
| 基金项目: |
| Author Name | Affiliation | E-mail | | Tong Zhu | GI Cancer Research Institute,Tongji Hospital,Huazhong University of Science and Technology,Wuhan,China | zhutong19990912@126.com | | Guihua Wang* | GI Cancer Research Institute,Tongji Hospital,Huazhong University of Science and Technology,Wuhan,China | ghwang@tjh.tjmu.edu.cn |
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| 中文摘要: |
|  Emerging data from metabolites-relating trails in cancers demonstrate that a common mechanism of
resistance to many novel classes of immune therapeutics is the emergence of immune escape due to the
reprogramming of cellular metabolism. Among them, current work about end-metabolites mostly focuses
on the intersection between lactate acid, adenosine, reactive oxygen species (ROS), and tumour immune
escape. In this article, we aim to review the evidence to date for the dynamic interplay between the three
end-metabolites and tumour immune escape for potential approaches to overcome obstacles in the efficacy
and durability of immune cancer therapies. We have organized known end-metabolites-associated immune
escape mechanisms into three hallmarks: (1) decreased immunogenicity of cancer cells which constitutes
defective antigen presentation and the attenuated expression of costimulatory molecules on tumour cells, (2)
immunosuppressive microenvironment with aberrant angiogenesis inhibits the differentiation, maturation,
and immune deviation of immune cells while drives the activation of immunosuppressive cells by immunesuppressive mediators (cytokines and other factors), (3) immune tolerance retained by inhibitory molecules
and depletion of immune cells. |
| 英文摘要: |
| Emerging data from metabolites-relating trails in cancers demonstrate that a common mechanism of
resistance to many novel classes of immune therapeutics is the emergence of immune escape due to the
reprogramming of cellular metabolism. Among them, current work about end-metabolites mostly focuses
on the intersection between lactate acid, adenosine, reactive oxygen species (ROS), and tumour immune
escape. In this article, we aim to review the evidence to date for the dynamic interplay between the three
end-metabolites and tumour immune escape for potential approaches to overcome obstacles in the efficacy
and durability of immune cancer therapies. We have organized known end-metabolites-associated immune
escape mechanisms into three hallmarks: (1) decreased immunogenicity of cancer cells which constitutes
defective antigen presentation and the attenuated expression of costimulatory molecules on tumour cells, (2)
immunosuppressive microenvironment with aberrant angiogenesis inhibits the differentiation, maturation,
and immune deviation of immune cells while drives the activation of immunosuppressive cells by immunesuppressive mediators (cytokines and other factors), (3) immune tolerance retained by inhibitory molecules
and depletion of immune cells. |
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