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Targeting myeloid villains in the treatment with immune checkpoint inhibitors in gastrointestinal cancer

Despite the clinical outcomes being extremely limited, blocking immune inhibitory checkpoint pathways has been in the spotlight as a promising strategy for treating gastrointestinal cancer. However, a distinct strategy for the successful treatment is obviously needed in the clinical settings. Myeloi...

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Autores principales: Kudo-Saito, Chie, Boku, Narikazu, Hirano, Hidekazu, Shoji, Hirokazu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9539086/
https://www.ncbi.nlm.nih.gov/pubmed/36211375
http://dx.doi.org/10.3389/fimmu.2022.1009701
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author Kudo-Saito, Chie
Boku, Narikazu
Hirano, Hidekazu
Shoji, Hirokazu
author_facet Kudo-Saito, Chie
Boku, Narikazu
Hirano, Hidekazu
Shoji, Hirokazu
author_sort Kudo-Saito, Chie
collection PubMed
description Despite the clinical outcomes being extremely limited, blocking immune inhibitory checkpoint pathways has been in the spotlight as a promising strategy for treating gastrointestinal cancer. However, a distinct strategy for the successful treatment is obviously needed in the clinical settings. Myeloid cells, such as neutrophils, macrophages, dendritic cells, and mast cells, are the majority of cellular components in the human immune system, but have received relatively less attention for the practical implementation than T cells and NK cells in cancer therapy because of concentration of the interest in development of the immune checkpoint blocking antibody inhibitors (ICIs). Abnormality of myeloid cells must impact on the entire host, including immune responses, stromagenesis, and cancer cells, leading to refractory cancer. This implies that elimination and reprogramming of the tumor-supportive myeloid villains may be a breakthrough to efficiently induce potent anti-tumor immunity in cancer patients. In this review, we provide an overview of current situation of the IC-blocking therapy of gastrointestinal cancer, including gastric, colorectal, and esophageal cancers. Also, we highlight the possible oncoimmunological components involved in the mechanisms underlying the resistance to the ICI therapy, particularly focusing on myeloid cells, including unique subsets expressing IC molecules. A deeper understanding of the molecular and cellular determinants may facilitate its practical implementation of targeting myeloid villains, and improve the clinical outcomes in the ICI therapy of gastrointestinal cancer.
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spelling pubmed-95390862022-10-08 Targeting myeloid villains in the treatment with immune checkpoint inhibitors in gastrointestinal cancer Kudo-Saito, Chie Boku, Narikazu Hirano, Hidekazu Shoji, Hirokazu Front Immunol Immunology Despite the clinical outcomes being extremely limited, blocking immune inhibitory checkpoint pathways has been in the spotlight as a promising strategy for treating gastrointestinal cancer. However, a distinct strategy for the successful treatment is obviously needed in the clinical settings. Myeloid cells, such as neutrophils, macrophages, dendritic cells, and mast cells, are the majority of cellular components in the human immune system, but have received relatively less attention for the practical implementation than T cells and NK cells in cancer therapy because of concentration of the interest in development of the immune checkpoint blocking antibody inhibitors (ICIs). Abnormality of myeloid cells must impact on the entire host, including immune responses, stromagenesis, and cancer cells, leading to refractory cancer. This implies that elimination and reprogramming of the tumor-supportive myeloid villains may be a breakthrough to efficiently induce potent anti-tumor immunity in cancer patients. In this review, we provide an overview of current situation of the IC-blocking therapy of gastrointestinal cancer, including gastric, colorectal, and esophageal cancers. Also, we highlight the possible oncoimmunological components involved in the mechanisms underlying the resistance to the ICI therapy, particularly focusing on myeloid cells, including unique subsets expressing IC molecules. A deeper understanding of the molecular and cellular determinants may facilitate its practical implementation of targeting myeloid villains, and improve the clinical outcomes in the ICI therapy of gastrointestinal cancer. Frontiers Media S.A. 2022-09-23 /pmc/articles/PMC9539086/ /pubmed/36211375 http://dx.doi.org/10.3389/fimmu.2022.1009701 Text en Copyright © 2022 Kudo-Saito, Boku, Hirano and Shoji https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Kudo-Saito, Chie
Boku, Narikazu
Hirano, Hidekazu
Shoji, Hirokazu
Targeting myeloid villains in the treatment with immune checkpoint inhibitors in gastrointestinal cancer
title Targeting myeloid villains in the treatment with immune checkpoint inhibitors in gastrointestinal cancer
title_full Targeting myeloid villains in the treatment with immune checkpoint inhibitors in gastrointestinal cancer
title_fullStr Targeting myeloid villains in the treatment with immune checkpoint inhibitors in gastrointestinal cancer
title_full_unstemmed Targeting myeloid villains in the treatment with immune checkpoint inhibitors in gastrointestinal cancer
title_short Targeting myeloid villains in the treatment with immune checkpoint inhibitors in gastrointestinal cancer
title_sort targeting myeloid villains in the treatment with immune checkpoint inhibitors in gastrointestinal cancer
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9539086/
https://www.ncbi.nlm.nih.gov/pubmed/36211375
http://dx.doi.org/10.3389/fimmu.2022.1009701
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