Autoren:	Bent, Rebekka Moll, Lorna Grabbe, Stephan Bros, Matthias
Titel:	Interleukin-1 beta - a friend or foe in malignancies?
Online-Publikationsdatum:	26-Nov-2018
Erscheinungsdatum:	2018
Sprache des Dokuments:	Englisch
Zusammenfassung/Abstract:	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.
DDC-Sachgruppe:	610 Medizin 610 Medical sciences
Veröffentlichende Institution:	Johannes Gutenberg-Universität Mainz
Organisationseinheit:	FB 04 Medizin
Veröffentlichungsort:	Mainz
ROR:	https://ror.org/023b0x485
DOI:	http://doi.org/10.25358/openscience-760
URN:	urn:nbn:de:hebis:77-publ-586594
Version:	Published version
Publikationstyp:	Zeitschriftenaufsatz
Nutzungsrechte:	CC BY
Informationen zu den Nutzungsrechten:	https://creativecommons.org/licenses/by/4.0/
Zeitschrift:	International journal of molecular sciences 19 8
Seitenzahl oder Artikelnummer:	Art. 2155
Verlag:	Molecular Diversity Preservation International
Verlagsort:	Basel
Erscheinungsdatum:	2018
ISSN:	1422-0067 1661-6596
URL der Originalveröffentlichung:	http://dx.doi.org/10.3390/ijms19082155
DOI der Originalveröffentlichung:	10.3390/ijms19082155
Enthalten in den Sammlungen:	JGU-Publikationen