Neurath M (2019)
Publication Type: Journal article, Review article
Publication year: 2019
Book Volume: 45
Pages Range: 1-8
DOI: 10.1016/j.cytogfr.2018.12.002
Studies in recent years have identified a pivotal role of the cytokine IL-23 in the pathogenesis of inflammatory bowel diseases (IBD: Crohn's disease, ulcerative colitis) and colitis-associated colon cancer. Genetic studies revealed that subgroups of IBD patients have single nucleotide polymorphisms in the IL-23R gene suggesting that IL-23R signaling affects disease susceptibility. Furthermore, increased production of IL-23 by macrophages, dendritic cells or granulocytes has been observed in various mouse models of colitis, colitis-associated cancer and IBD patients. Moreover, in several murine models of colitis, suppression of IL-12/IL-23 p40, IL-23 p19 or IL-23R function led to marked suppression of gut inflammation. This finding was associated with reduced activation of IL-23 target cells such as T helper 17 cells, innate lymphoid cells type 3, granulocytes and natural killer cells as well as with impaired production of proinflammatory cytokines. Based on these findings, targeting of IL-23 emerges as important concept for suppression of gut inflammation and inflammation-associated cancer growth. Consistently, neutralizing antibodies against IL-12/IL-23 p40 and IL-23 p19 have been successfully used in clinical trials for therapy of Crohn's disease and pilot studies in ulcerative colitis are ongoing. These findings underline the crucial regulatory role of IL-23 in chronic intestinal inflammation and colitis-associated cancer and indicate that therapeutic strategies aiming at IL-23 blockade may be of key relevance for future therapy of IBD patients.
APA:
Neurath, M. (2019). IL-23 in inflammatory bowel diseases and colon cancer. Cytokine & Growth Factor Reviews, 45, 1-8. https://doi.org/10.1016/j.cytogfr.2018.12.002
MLA:
Neurath, Markus. "IL-23 in inflammatory bowel diseases and colon cancer." Cytokine & Growth Factor Reviews 45 (2019): 1-8.
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