L’IL-23R, un nouveau gène de susceptibilité dans les maladies inflammatoires chroniques intestinales

Laurent Peyrin-Biroulet; Erika Parmentier-Decrucq; Julien Branche; Pierre Desreumaux

doi:10.1051/medsci/2007233250

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Volume 23 / No 3 (Mars 2007)

Med Sci (Paris), 23 3 (2007) 250-252

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Issue		Med Sci (Paris) Volume 23, Number 3, Mars 2007


Page(s)		250 - 252
Section		Nouvelles
DOI		https://doi.org/10.1051/medsci/2007233250
Published online		15 March 2007

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Hue S, Ahern P, Buonocore S, et al. Interleukin-23 drives innate and T cell-mediated intestinal inflammation. J Exp Med 2006; 203 : 2473–83. [Google Scholar]
Yen D, Cheung J, Scheerens H, et al. IL-23 is essential for T cell-mediated colitis and promotes inflammation via IL-17 and IL-6. J Clin Invest 2006; 116 : 1310–6. [Google Scholar]
Mangan PR, Harrington LE, O’Quinn DB, et al. Transforming growth factor-beta induces development of the T(H)17 lineage. Nature 2006; 441 : 231–4. [Google Scholar]
Verreck FA, de Boer T, Langenberg DM, et al. Human IL-23-producing type 1 macrophages promote but IL-10-producing type 2 macrophages subvert immunity to (myco)bacteria. Proc Natl Acad Sci USA 2004; 101 : 4560–5. [Google Scholar]
Cooper AM, Kipnis A, Turner J, et al. Mice lacking bioactive IL-12 can generate protective, antigen-specific cellular responses to mycobacterial infection only if the IL-12 p40 subunit is present. J Immunol 2002; 168 : 1322–7. [Google Scholar]

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[1] Halme L, Paavola-Sakki P, Turunen U, et al. Family and twin studies in inflammatory bowel disease. World J Gastroenterol 2006; 12 : 3668–72. [Google Scholar]

[2] Tysk C, Lindberg E, Jarnerot G, Floderus-Myrhed B. Ulcerative colitis and Crohn’s disease in an unselected population of monozygotic and dizygotic twins. A study of heritability and the influence of smoking. Gut 1988; 29 : 990–6. [Google Scholar]

[3] Hugot JP, Chamaillard M, Zouali H, et al. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn’s disease. Nature 2001; 411 : 599–603. [Google Scholar]

[4] Ogura Y, Bonen DK, Inohara N, et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn’s disease. Nature 2001; 411 : 603–6. [Google Scholar]

[5] Chamaillard M, Iacob R, Desreumaux P, Colombel JF. Advances and perspectives in the genetics of inflammatory bowel diseases. Clin Gastroenterol Hepatol 2006; 4 :143–51. [Google Scholar]

[6] Duerr RH, Taylor KD, Brant SR, et al. A genome-wide association study identifies IL23R as an inflammatory bowel disease gene. Science 2006; 314 : 1461–3. [Google Scholar]

[7] Hue S, Ahern P, Buonocore S, et al. Interleukin-23 drives innate and T cell-mediated intestinal inflammation. J Exp Med 2006; 203 : 2473–83. [Google Scholar]

[8] Yen D, Cheung J, Scheerens H, et al. IL-23 is essential for T cell-mediated colitis and promotes inflammation via IL-17 and IL-6. J Clin Invest 2006; 116 : 1310–6. [Google Scholar]

[9] Mangan PR, Harrington LE, O’Quinn DB, et al. Transforming growth factor-beta induces development of the T(H)17 lineage. Nature 2006; 441 : 231–4. [Google Scholar]

[10] Verreck FA, de Boer T, Langenberg DM, et al. Human IL-23-producing type 1 macrophages promote but IL-10-producing type 2 macrophages subvert immunity to (myco)bacteria. Proc Natl Acad Sci USA 2004; 101 : 4560–5. [Google Scholar]

[11] Cooper AM, Kipnis A, Turner J, et al. Mice lacking bioactive IL-12 can generate protective, antigen-specific cellular responses to mycobacterial infection only if the IL-12 p40 subunit is present. J Immunol 2002; 168 : 1322–7. [Google Scholar]