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CD47/SIRPα axis: bridging innate and adaptive immunity
Myeloid immune cells are frequently present in the tumor environment, and although they can positively contribute to tumor control they often negatively impact anticancer immune responses. One way of inhibiting the positive contributions of myeloid cells is by signaling through the cluster of differ...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BMJ Publishing Group
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9280883/ https://www.ncbi.nlm.nih.gov/pubmed/35831032 http://dx.doi.org/10.1136/jitc-2022-004589 |
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author | van Duijn, Anneloes Van der Burg, Sjoerd H Scheeren, Ferenc A |
author_facet | van Duijn, Anneloes Van der Burg, Sjoerd H Scheeren, Ferenc A |
author_sort | van Duijn, Anneloes |
collection | PubMed |
description | Myeloid immune cells are frequently present in the tumor environment, and although they can positively contribute to tumor control they often negatively impact anticancer immune responses. One way of inhibiting the positive contributions of myeloid cells is by signaling through the cluster of differentiation 47 (CD47)/signal regulatory protein alpha (SIRPα) axis. The SIRPα receptor is expressed on myeloid cells and is an inhibitory immune receptor that, upon binding to CD47 protein, delivers a ‘don’t eat me’ signal. As CD47 is often overexpressed on cancer cells, treatments targeting CD47/SIRPα have been under active investigation and are currently being tested in clinical settings. Interestingly, the CD47/SIRPα axis is also involved in T cell-mediated antitumor responses. In this perspective we provide an overview of recent studies showing how therapeutic blockade of the CD47/SIRPα axis improves the adaptive immune response. Furthermore, we discuss the interconnection between the myeloid CD47/SIRPα axis and adaptive T cell responses as well as the potential therapeutic role of the CD47/SIRPα axis in tumors with acquired resistance to the classic immunotherapy through major histocompatibility complex downregulation. Altogether this review provides a profound insight for the optimal exploitation of CD47/SIRPα immune checkpoint therapy. |
format | Online Article Text |
id | pubmed-9280883 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BMJ Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-92808832022-07-28 CD47/SIRPα axis: bridging innate and adaptive immunity van Duijn, Anneloes Van der Burg, Sjoerd H Scheeren, Ferenc A J Immunother Cancer Review Myeloid immune cells are frequently present in the tumor environment, and although they can positively contribute to tumor control they often negatively impact anticancer immune responses. One way of inhibiting the positive contributions of myeloid cells is by signaling through the cluster of differentiation 47 (CD47)/signal regulatory protein alpha (SIRPα) axis. The SIRPα receptor is expressed on myeloid cells and is an inhibitory immune receptor that, upon binding to CD47 protein, delivers a ‘don’t eat me’ signal. As CD47 is often overexpressed on cancer cells, treatments targeting CD47/SIRPα have been under active investigation and are currently being tested in clinical settings. Interestingly, the CD47/SIRPα axis is also involved in T cell-mediated antitumor responses. In this perspective we provide an overview of recent studies showing how therapeutic blockade of the CD47/SIRPα axis improves the adaptive immune response. Furthermore, we discuss the interconnection between the myeloid CD47/SIRPα axis and adaptive T cell responses as well as the potential therapeutic role of the CD47/SIRPα axis in tumors with acquired resistance to the classic immunotherapy through major histocompatibility complex downregulation. Altogether this review provides a profound insight for the optimal exploitation of CD47/SIRPα immune checkpoint therapy. BMJ Publishing Group 2022-07-13 /pmc/articles/PMC9280883/ /pubmed/35831032 http://dx.doi.org/10.1136/jitc-2022-004589 Text en © Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. https://creativecommons.org/licenses/by-nc/4.0/This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) . |
spellingShingle | Review van Duijn, Anneloes Van der Burg, Sjoerd H Scheeren, Ferenc A CD47/SIRPα axis: bridging innate and adaptive immunity |
title | CD47/SIRPα axis: bridging innate and adaptive immunity |
title_full | CD47/SIRPα axis: bridging innate and adaptive immunity |
title_fullStr | CD47/SIRPα axis: bridging innate and adaptive immunity |
title_full_unstemmed | CD47/SIRPα axis: bridging innate and adaptive immunity |
title_short | CD47/SIRPα axis: bridging innate and adaptive immunity |
title_sort | cd47/sirpα axis: bridging innate and adaptive immunity |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9280883/ https://www.ncbi.nlm.nih.gov/pubmed/35831032 http://dx.doi.org/10.1136/jitc-2022-004589 |
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