IL-23 is essential for T cell-mediated colitis and promotes inflammation via IL-17 and IL-6.
By D. Yen, J. Cheung, H. Scheerens, F. Poulet, T. Mcclanahan, Brent S. McKenzie, M. Kleinschek, Alexander M. Owyang, J. Mattson, W. Blumenschein and 5 more. 2006
1,659 citations recorded by the source corpus.
Subfields: Genetics, Immunology
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Genetics
In Immunology
Citations in the corpus
- Interleukin-23 drives innate and T cell–mediated intestinal inflammation (2006, background): “Although this was associated with increased development of pathogenic Th17 cells, anti–IL-17 treatment had little impact on colitis and had to be combined with anti–IL-6 treatment to attenuate disease (42).”
- IL-22 ameliorates intestinal inflammation in a mouse model of ulcerative colitis. (2008, background): “In contrast, IL-23/IL-17 pathways have recently been shown to play a pathogenic role in experimental CD-like diseases (15, 16, 47, 48).”
- TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27/STAT1 (2007, background): “IL-23 drives the expansion of T H 17 cells, which produce IL-17, IL-6 and TNF-α, and are now recognized as causative agents of several diseases previously attributed to T H 1 cell”
- IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses (2011, background): “Both the T H 1 subset and the T H 17 subset promote cellular immune function and can cause inflammation and autoimmune diseases, such as inflammatory bowel disease and collagen-induce arthriti”
- The IL-23/Th17 axis in the immunopathogenesis of psoriasis. (2009, background): “Furthermore, the development of spontaneous colitis in IL-10-deficient mice is completely prevented by crossing them with IL-23p19-deficient mice (Yen et al., 2006).”
- Th17 cells in human disease (2008, background): “IL-23 upregulates IL-17 production and promotes survival and expansion of activated or memory Th17 cells in vitro, although it is not absolutely necessary (8, 12, 22).”