The IL23 axis plays a key role in the pathogenesis of IBD

被引：167

作者：

McGovern, Dermot ^{[1
]}

Powrie, Fiona ^{[1
]}

机构：

[1] Hammersmith Hosp, Imperial Coll, London W12 0HS, England

来源：

GUT | 2007年 / 56卷 / 10期

关键词：

D O I：

10.1136/gut.2006.115402

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

Exciting new results from a genetic study in humans and functional studies in mice have pinpointed interleukin 23 (IL23) and its receptor as a key pathway in the pathogenesis of inflammatory bowel disease (IBD). These findings reveal a hitherto unappreciated role for the IL23 axis in intestinal inflammation and may open new avenues for development of therapeutic strategies in IBD.

引用

页码：1333 / 1336

页数：4

共 35 条

[1] Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17 [J].

Aggarwal, S ;

Ghilardi, N ;

Xie, MH ;

de Sauvage, FJ ;

Gurney, AL .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (03) :1910-1914

[2] The molecular classification of the clinical manifestations of Crohn's disease [J].

Ahmad, T ;

Armuzzi, A ;

Bunce, M ;

Mulcahy-Hawes, K ;

Marshall, SE ;

Orchard, TR ;

Crawshaw, J ;

Large, O ;

De Silva, A ;

Cook, JT ;

Barnardo, M ;

Cullen, S ;

Welsh, KI ;

Jewell, DP .

GASTROENTEROLOGY, 2002, 122 (04) :854-866

[3] Constitutive p40 promoter activation and IL-23 production in the terminal ileum mediated by dendritic cells [J].

Becker, C ;

Wirtz, S ;

Blessing, M ;

Pirhonen, J ;

Strand, D ;

Bechthold, O ;

Frick, J ;

Galle, PR ;

Autenrieth, I ;

Neurath, MF .

JOURNAL OF CLINICAL INVESTIGATION, 2003, 112 (05) :693-706

[4] Cutting edge: IL-23 cross-regulates IL-12 production in T cell-dependent experimental colitis [J].

Becker, Christoph ;

Dornhoff, Heike ;

Neufert, Clemens ;

Fantini, Massimo C. ;

Wirtz, Stefan ;

Huebner, Sabine ;

Nikolaev, Alexei ;

Lehr, Hans-Anton ;

Murphy, Andrew J. ;

Valenzuela, David M. ;

Yancopoulos, George D. ;

Galle, Peter R. ;

Karow, Margaret ;

Neurath, Markus F. .

JOURNAL OF IMMUNOLOGY, 2006, 177 (05) :2760-2764

[5] The immunological and genetic basis of inflammatory bowel disease [J].

Bouma, G ;

Strober, W .

NATURE REVIEWS IMMUNOLOGY, 2003, 3 (07) :521-533

[6] Anti-IL-23 therapy inhibits multiple inflammatory pathways and ameliorates autoimmune encephalomyelitis [J].

Chen, Y ;

Langrish, CL ;

Mckenzie, B ;

Joyce-Shaikh, B ;

Stumhofer, JS ;

McClanahan, T ;

Blumenschein, W ;

Churakovsa, T ;

Low, J ;

Presta, L ;

Hunter, CA ;

Kastelein, RA ;

Cua, DJ .

JOURNAL OF CLINICAL INVESTIGATION, 2006, 116 (05) :1317-1326

[7] Identification of novel susceptibility loci for inflammatory bowel disease on chromosomes 1q, 3q, and 4q:: Evidence for epistasis between 1p and IBD1 [J].

Cho, JH ;

Nicolae, DL ;

Gold, LH ;

Fields, CT ;

LaBuda, MC ;

Rohal, PM ;

Pickles, MR ;

Qin, L ;

Fu, YF ;

Mann, JS ;

Kirschner, BS ;

Jabs, EW ;

Weber, J ;

Hanauer, SB ;

Bayless, TM ;

Brant, SR .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (13) :7502-7507

[8] Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain [J].

Cua, DJ ;

Sherlock, J ;

Chen, Y ;

Murphy, CA ;

Joyce, B ;

Seymour, B ;

Lucian, L ;

To, W ;

Kwan, S ;

Churakova, T ;

Zurawski, S ;

Wiekowski, M ;

Lira, SA ;

Gorman, D ;

Kastelein, RA ;

Sedgwick, JD .

NATURE, 2003, 421 (6924) :744-748

[9] A genome-wide association study identifies IL23R as an inflammatory bowel disease gene [J].

Duerr, Richard H. ;

Taylor, Kent D. ;

Brant, Steven R. ;

Rioux, John D. ;

Silverberg, Mark S. ;

Daly, Mark J. ;

Steinhart, A. Hillary ;

Abraham, Clara ;

Regueiro, Miguel ;

Griffiths, Anne ;

Dassopoulos, Themistocles ;

Bitton, Alain ;

Yang, Huiying ;

Targan, Stephan ;

Datta, Lisa Wu ;

Kistner, Emily O. ;

Schumm, L. Philip ;

Lee, Annette T. ;

Gregersen, Peter K. ;

Barmada, M. Michael ;

Rotter, Jerome I. ;

Nicolae, Dan L. ;

Cho, Judy H. .

SCIENCE, 2006, 314 (5804) :1461-1463

[10] Increased expression of interleukin 17 in inflammatory bowel disease [J].

Fujino, S ;

Andoh, A ;

Bamba, S ;

Ogawa, A ;

Hata, K ;

Araki, Y ;

Bamba, T ;

Fujiyama, Y .

GUT, 2003, 52 (01) :65-70

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