{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T16:35:12Z","timestamp":1792427712820,"version":"4.5.0"},"reference-count":297,"publisher":"MDPI AG","issue":"8","license":[{"start":{"date-parts":[[2018,7,24]],"date-time":"2018-07-24T00:00:00Z","timestamp":1532390400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Interleukin-1 beta (IL-1\u03b2) is induced by inflammatory signals in a broad number of immune cell types. IL-1\u03b2 (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-1\u03b2 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-1\u03b2 has been attributed a largely beneficial role in resolving acute inflammations, and by initiating adaptive anti-tumor responses. However, IL-1\u03b2 generated in the course of chronic inflammation supports tumor development. Furthermore, IL-1\u03b2 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-1\u03b2 is a driver of tumor induction and development.<\/jats:p>","DOI":"10.3390\/ijms19082155","type":"journal-article","created":{"date-parts":[[2018,7,24]],"date-time":"2018-07-24T11:51:38Z","timestamp":1532433098000},"page":"2155","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":416,"title":["Interleukin-1 Beta\u2014A Friend or Foe in Malignancies?"],"prefix":"10.3390","volume":"19","author":[{"given":"Rebekka","family":"Bent","sequence":"first","affiliation":[{"name":"Department of Dermatology, University Medical Center, 55131 Mainz, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lorna","family":"Moll","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University Medical Center, 55131 Mainz, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephan","family":"Grabbe","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University Medical Center, 55131 Mainz, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Bros","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University Medical Center, 55131 Mainz, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2018,7,24]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"S43","DOI":"10.2119\/molmed.2014.00232","article-title":"An expanding role for interleukin-1 blockade from gout to cancer","volume":"20","author":"Dinarello","year":"2014","journal-title":"Mol. 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