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Understanding Inflammasomes and PD-1/PD-L1 Crosstalk to Improve Cancer Treatment Efficiency
SIMPLE SUMMARY: Immune checkpoints and inflammasomes have been shown to regulate cancer progression and response to treatments. This review summarizes the recent findings on the crosstalk between the immune checkpoint PD-1 and inflammasomes and the promising association of treatments that might be e...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7761387/ https://www.ncbi.nlm.nih.gov/pubmed/33261061 http://dx.doi.org/10.3390/cancers12123550 |
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author | Perrichet, Anaïs Ghiringhelli, François Rébé, Cédric |
author_facet | Perrichet, Anaïs Ghiringhelli, François Rébé, Cédric |
author_sort | Perrichet, Anaïs |
collection | PubMed |
description | SIMPLE SUMMARY: Immune checkpoints and inflammasomes have been shown to regulate cancer progression and response to treatments. This review summarizes the recent findings on the crosstalk between the immune checkpoint PD-1 and inflammasomes and the promising association of treatments that might be efficient for cancer patients. ABSTRACT: Inflammasomes and immune checkpoints have been shown to participate in carcinogenesis, cancer growth and response to treatment. Thus, targeting cytokines resulting from inflammasome activation, such as interleukin (IL)-1β, has emerged as a new tool in the therapeutic arsenal. Moreover, the use of checkpoint inhibitors such as anti-PD-1 or anti-PD-L1 has revolutionized the treatment of some cancer patients. However, inflammasome activation and consecutive cytokine release only occurs in some chemotherapeutic treatments and immune checkpoint inhibitors only work for a restricted number of patients, thus limiting the use of therapies targeting these pathways. Expanding knowledge about the inefficiency of these therapies recently brought forward the hypothesis of targeting both pathways. In this review, we provide an overview of the crosstalk between inflammasomes and programmed death-1 (PD-1)/programmed death-ligand 1 (PD-L1) that might explain how these two pathways are mutually dependent, and perhaps why targeting only one of them leads to inefficiency of cancer treatment in some patients. |
format | Online Article Text |
id | pubmed-7761387 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-77613872020-12-26 Understanding Inflammasomes and PD-1/PD-L1 Crosstalk to Improve Cancer Treatment Efficiency Perrichet, Anaïs Ghiringhelli, François Rébé, Cédric Cancers (Basel) Review SIMPLE SUMMARY: Immune checkpoints and inflammasomes have been shown to regulate cancer progression and response to treatments. This review summarizes the recent findings on the crosstalk between the immune checkpoint PD-1 and inflammasomes and the promising association of treatments that might be efficient for cancer patients. ABSTRACT: Inflammasomes and immune checkpoints have been shown to participate in carcinogenesis, cancer growth and response to treatment. Thus, targeting cytokines resulting from inflammasome activation, such as interleukin (IL)-1β, has emerged as a new tool in the therapeutic arsenal. Moreover, the use of checkpoint inhibitors such as anti-PD-1 or anti-PD-L1 has revolutionized the treatment of some cancer patients. However, inflammasome activation and consecutive cytokine release only occurs in some chemotherapeutic treatments and immune checkpoint inhibitors only work for a restricted number of patients, thus limiting the use of therapies targeting these pathways. Expanding knowledge about the inefficiency of these therapies recently brought forward the hypothesis of targeting both pathways. In this review, we provide an overview of the crosstalk between inflammasomes and programmed death-1 (PD-1)/programmed death-ligand 1 (PD-L1) that might explain how these two pathways are mutually dependent, and perhaps why targeting only one of them leads to inefficiency of cancer treatment in some patients. MDPI 2020-11-27 /pmc/articles/PMC7761387/ /pubmed/33261061 http://dx.doi.org/10.3390/cancers12123550 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Perrichet, Anaïs Ghiringhelli, François Rébé, Cédric Understanding Inflammasomes and PD-1/PD-L1 Crosstalk to Improve Cancer Treatment Efficiency |
title | Understanding Inflammasomes and PD-1/PD-L1 Crosstalk to Improve Cancer Treatment Efficiency |
title_full | Understanding Inflammasomes and PD-1/PD-L1 Crosstalk to Improve Cancer Treatment Efficiency |
title_fullStr | Understanding Inflammasomes and PD-1/PD-L1 Crosstalk to Improve Cancer Treatment Efficiency |
title_full_unstemmed | Understanding Inflammasomes and PD-1/PD-L1 Crosstalk to Improve Cancer Treatment Efficiency |
title_short | Understanding Inflammasomes and PD-1/PD-L1 Crosstalk to Improve Cancer Treatment Efficiency |
title_sort | understanding inflammasomes and pd-1/pd-l1 crosstalk to improve cancer treatment efficiency |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7761387/ https://www.ncbi.nlm.nih.gov/pubmed/33261061 http://dx.doi.org/10.3390/cancers12123550 |
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