The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.
Interleukin-1 Beta—A Friend or Foe in Malignancies?
Open accessAbstract
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.
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Metadata
- Authors
- Bent, R., Moll, L., Grabbe, S., & Bros, M.
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2018-07-24
- Volume
- 19
- Issue
- 8
- Pages
- 2155
- ISSN
- 1422-0067 (ISSN-L)
- OpenAlex
- W2883276763
- Cited by
- 444
- References
- 26
- FWCI
- 10.36
- Type
- journal article
- Language
- en
- Open access
- gold
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