Interleukin 23
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Interleukin-23 (IL-23) is a heterodimeric cytokine consisting of two subunits, one called p40, which is shared with another cytokine, IL-12, and another called p19 (the IL-23 alpha subunit). IL-23 is an important part of the inflammatory response against infection. It promotes upregulation of the matrix metalloprotease MMP9, increases angiogenesis and reduces CD8+ T-cell infiltration. Recently, IL-23 has been implicated in the development of cancerous tumors. In conjunction with IL-6 and TGF-β1, IL-23 stimulates naive CD4+ T cells to differentiate into a novel subset of cells called Th17 cells, which are distinct from the classical Th1 and Th2 cells. Th17 cells produce IL-17, a proinflammatory cytokine that enhances T cell priming and stimulates the production of proinflammatory molecules such as IL-1, IL-6, TNF-alpha, NOS-2, and chemokines resulting in inflammation. Knockout mice deficient in either p40 or p19, or in either subunit of the IL-23 receptor (IL-23R and IL12R-β1) develop less severe symptoms of multiple sclerosis and inflammatory bowel disease highlighting the importance of IL-23 in the inflammatory pathway[1][2]. Entheseal-resident T cells are sensitive to IL-23 overexpression and they respond vigorously by releasing IL-17 and IL-22 which lead to local inflammatory changes and osteoblast-mediated bone remodeling. These T cells are also present in the aortic root and valve, leading to aortitis that may be seen in patients with ankylosing spondylitis.
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References
- ↑ http://www.nature.com/nature/journal/v442/n7101/full/nature04808.html
- ↑ Kristine Kikly, Ling Liu, Songqing Na and Jonathon D Sedgwick. The IL-23/Th(17) axis: therapeutic targets for autoimmune inflammation. Curr Opin Immunol. 2006, Volume 18, pages 670-5.