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Interleukin-1 Beta—A Friend or Foe in Malignancies?
Interleukin-1 beta (IL-1β) is induced by inflammatory signals in a broad number of immune cell types. IL-1β (and IL-18) are the only cytokines which are processed by caspase-1 after inflammasome-mediated activation. This review aims to summarize current knowledge about parameters of regulation of IL...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6121377/ https://www.ncbi.nlm.nih.gov/pubmed/30042333 http://dx.doi.org/10.3390/ijms19082155 |
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author | Bent, Rebekka Moll, Lorna Grabbe, Stephan Bros, Matthias |
author_facet | Bent, Rebekka Moll, Lorna Grabbe, Stephan Bros, Matthias |
author_sort | Bent, Rebekka |
collection | PubMed |
description | Interleukin-1 beta (IL-1β) is induced by inflammatory signals in a broad number of immune cell types. IL-1β (and IL-18) are the only cytokines which are processed by caspase-1 after inflammasome-mediated activation. This review aims to summarize current knowledge about parameters of regulation of IL-1β expression and its multi-facetted role in pathophysiological conditions. IL-1 signaling activates innate immune cells including antigen presenting cells, and drives polarization of CD4+ T cells towards T helper type (Th) 1 and Th17 cells. Therefore, IL-1β has been attributed a largely beneficial role in resolving acute inflammations, and by initiating adaptive anti-tumor responses. However, IL-1β generated in the course of chronic inflammation supports tumor development. Furthermore, IL-1β generated within the tumor microenvironment predominantly by tumor-infiltrating macrophages promotes tumor growth and metastasis via different mechanisms. These include the expression of IL-1 targets which promote neoangiogenesis and of soluble mediators in cancer-associated fibroblasts that evoke antiapoptotic signaling in tumor cells. Moreover, IL-1 promotes the propagation of myeloid-derived suppressor cells. Using genetic mouse models as well as agents for pharmacological inhibition of IL-1 signaling therapeutically applied for treatment of IL-1 associated autoimmune diseases indicate that IL-1β is a driver of tumor induction and development. |
format | Online Article Text |
id | pubmed-6121377 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-61213772018-09-07 Interleukin-1 Beta—A Friend or Foe in Malignancies? Bent, Rebekka Moll, Lorna Grabbe, Stephan Bros, Matthias Int J Mol Sci Review Interleukin-1 beta (IL-1β) is induced by inflammatory signals in a broad number of immune cell types. IL-1β (and IL-18) are the only cytokines which are processed by caspase-1 after inflammasome-mediated activation. This review aims to summarize current knowledge about parameters of regulation of IL-1β expression and its multi-facetted role in pathophysiological conditions. IL-1 signaling activates innate immune cells including antigen presenting cells, and drives polarization of CD4+ T cells towards T helper type (Th) 1 and Th17 cells. Therefore, IL-1β has been attributed a largely beneficial role in resolving acute inflammations, and by initiating adaptive anti-tumor responses. However, IL-1β generated in the course of chronic inflammation supports tumor development. Furthermore, IL-1β generated within the tumor microenvironment predominantly by tumor-infiltrating macrophages promotes tumor growth and metastasis via different mechanisms. These include the expression of IL-1 targets which promote neoangiogenesis and of soluble mediators in cancer-associated fibroblasts that evoke antiapoptotic signaling in tumor cells. Moreover, IL-1 promotes the propagation of myeloid-derived suppressor cells. Using genetic mouse models as well as agents for pharmacological inhibition of IL-1 signaling therapeutically applied for treatment of IL-1 associated autoimmune diseases indicate that IL-1β is a driver of tumor induction and development. MDPI 2018-07-24 /pmc/articles/PMC6121377/ /pubmed/30042333 http://dx.doi.org/10.3390/ijms19082155 Text en © 2018 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 Bent, Rebekka Moll, Lorna Grabbe, Stephan Bros, Matthias Interleukin-1 Beta—A Friend or Foe in Malignancies? |
title | Interleukin-1 Beta—A Friend or Foe in Malignancies? |
title_full | Interleukin-1 Beta—A Friend or Foe in Malignancies? |
title_fullStr | Interleukin-1 Beta—A Friend or Foe in Malignancies? |
title_full_unstemmed | Interleukin-1 Beta—A Friend or Foe in Malignancies? |
title_short | Interleukin-1 Beta—A Friend or Foe in Malignancies? |
title_sort | interleukin-1 beta—a friend or foe in malignancies? |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6121377/ https://www.ncbi.nlm.nih.gov/pubmed/30042333 http://dx.doi.org/10.3390/ijms19082155 |
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