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Interactions between tumor-derived proteins and Toll-like receptors
Damage-associated molecular patterns (DAMPs) are danger signals (or alarmins) alerting immune cells through pattern recognition receptors (PRRs) to begin defense activity. Moreover, DAMPs are host biomolecules that can initiate a noninflammatory response to infection, and pathogen-associated molecul...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8080774/ https://www.ncbi.nlm.nih.gov/pubmed/33299138 http://dx.doi.org/10.1038/s12276-020-00540-4 |
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author | Jang, Gun-Young Lee, Ji won Kim, Young Seob Lee, Sung Eun Han, Hee Dong Hong, Kee-Jong Kang, Tae Heung Park, Yeong-Min |
author_facet | Jang, Gun-Young Lee, Ji won Kim, Young Seob Lee, Sung Eun Han, Hee Dong Hong, Kee-Jong Kang, Tae Heung Park, Yeong-Min |
author_sort | Jang, Gun-Young |
collection | PubMed |
description | Damage-associated molecular patterns (DAMPs) are danger signals (or alarmins) alerting immune cells through pattern recognition receptors (PRRs) to begin defense activity. Moreover, DAMPs are host biomolecules that can initiate a noninflammatory response to infection, and pathogen-associated molecular pattern (PAMPs) perpetuate the inflammatory response to infection. Many DAMPs are proteins that have defined intracellular functions and are released from dying cells after tissue injury or chemo-/radiotherapy. In the tumor microenvironment, DAMPs can be ligands for Toll-like receptors (TLRs) expressed on immune cells and induce cytokine production and T-cell activation. Moreover, DAMPs released from tumor cells can directly activate tumor-expressed TLRs that induce chemoresistance, migration, invasion, and metastasis. Furthermore, DAMP-induced chronic inflammation in the tumor microenvironment causes an increase in immunosuppressive populations, such as M2 macrophages, myeloid-derived suppressor cells (MDSCs), and regulatory T cells (Tregs). Therefore, regulation of DAMP proteins can reduce excessive inflammation to create an immunogenic tumor microenvironment. Here, we review tumor-derived DAMP proteins as ligands of TLRs and discuss their association with immune cells, tumors, and the composition of the tumor microenvironment. |
format | Online Article Text |
id | pubmed-8080774 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-80807742021-04-29 Interactions between tumor-derived proteins and Toll-like receptors Jang, Gun-Young Lee, Ji won Kim, Young Seob Lee, Sung Eun Han, Hee Dong Hong, Kee-Jong Kang, Tae Heung Park, Yeong-Min Exp Mol Med Review Article Damage-associated molecular patterns (DAMPs) are danger signals (or alarmins) alerting immune cells through pattern recognition receptors (PRRs) to begin defense activity. Moreover, DAMPs are host biomolecules that can initiate a noninflammatory response to infection, and pathogen-associated molecular pattern (PAMPs) perpetuate the inflammatory response to infection. Many DAMPs are proteins that have defined intracellular functions and are released from dying cells after tissue injury or chemo-/radiotherapy. In the tumor microenvironment, DAMPs can be ligands for Toll-like receptors (TLRs) expressed on immune cells and induce cytokine production and T-cell activation. Moreover, DAMPs released from tumor cells can directly activate tumor-expressed TLRs that induce chemoresistance, migration, invasion, and metastasis. Furthermore, DAMP-induced chronic inflammation in the tumor microenvironment causes an increase in immunosuppressive populations, such as M2 macrophages, myeloid-derived suppressor cells (MDSCs), and regulatory T cells (Tregs). Therefore, regulation of DAMP proteins can reduce excessive inflammation to create an immunogenic tumor microenvironment. Here, we review tumor-derived DAMP proteins as ligands of TLRs and discuss their association with immune cells, tumors, and the composition of the tumor microenvironment. Nature Publishing Group UK 2020-12-09 /pmc/articles/PMC8080774/ /pubmed/33299138 http://dx.doi.org/10.1038/s12276-020-00540-4 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Review Article Jang, Gun-Young Lee, Ji won Kim, Young Seob Lee, Sung Eun Han, Hee Dong Hong, Kee-Jong Kang, Tae Heung Park, Yeong-Min Interactions between tumor-derived proteins and Toll-like receptors |
title | Interactions between tumor-derived proteins and Toll-like receptors |
title_full | Interactions between tumor-derived proteins and Toll-like receptors |
title_fullStr | Interactions between tumor-derived proteins and Toll-like receptors |
title_full_unstemmed | Interactions between tumor-derived proteins and Toll-like receptors |
title_short | Interactions between tumor-derived proteins and Toll-like receptors |
title_sort | interactions between tumor-derived proteins and toll-like receptors |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8080774/ https://www.ncbi.nlm.nih.gov/pubmed/33299138 http://dx.doi.org/10.1038/s12276-020-00540-4 |
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