Animal models of IBD: linkage to human disease.
Animal models of IBD: linkage to human disease.
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DOI：
10.1016/j.coph.2010.05.007
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发表时间：
2010-10
影响因子：
4
通讯作者：
Mizoguchi, Emiko
中科院分区：
文献类型：
--
作者：
Mizoguchi, Atsushi;Mizoguchi, Emiko
在许多不同种类的基因工程小鼠中肠道炎症的自发发展以及人类中许多易感基因的存在表明，炎症性肠病（IBD）是由比以前预测的更复杂的机制介导的。人类遗传学研究揭示了IBD发病机制中的一些主要途径，包括上皮对肠道微生物群的防御、IL-23/Th 17轴和免疫调节。已经产生了经遗传工程改造以缺乏某些易感基因的小鼠IBD模型，并且已经提供了对IBD的直接靶向易感基因或间接靶向其下游通路的治疗潜力的有用见解。本文综述了目前有关IBD相关基因的功能，来自基因工程小鼠模型的信息。
Spontaneous development of intestinal inflammation in many different kinds of genetically engineered mice as well as the presence of numerous susceptibility genes in humans suggests that inflammatory bowel disease (IBD) is mediated by more complicated mechanisms than previously predicted. The human genetic studies implicate some major pathways in the pathogenesis of IBD, including epithelial defense against commensal microbiota, the IL-23/Th17 axis, and immune regulation. Murine IBD models, which are genetically engineered to lack some susceptibility genes, have been generated, and have provided useful insights into the therapeutic potential of targeting the susceptibility genes directly or their downstream pathways indirectly for IBD. This review summarizes current information related to the function of IBD-associated genes as derived from genetically engineered mouse models.
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DOI：
10.1084/jem.20070663
发表时间：
2007-08-06
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Annunziato F;Cosmi L;Santarlasci V;Maggi L;Liotta F;Mazzinghi B;Parente E;Filì L;Ferri S;Frosali F;Giudici F;Romagnani P;Parronchi P;Tonelli F;Maggi E;Romagnani S
通讯作者：
Romagnani S
影响因子：
29.4
作者：
Fina, Daniele;Sarra, Massimiliano;Monteleone, Giovanni
通讯作者：
Monteleone, Giovanni
影响因子：
56.9
作者：
Duerr, Richard H.;Taylor, Kent D.;Cho, Judy H.
通讯作者：
Cho, Judy H.
影响因子：
30.8
作者：
Barrett, Jeffrey C.;Lee, James C.;Lees, Charles W.;Prescott, Natalie J.;Anderson, Carl A.;Phillips, Anne;Wesley, Emma;Parnell, Kirstie;Zhang, Hu;Drummond, Hazel;Nimmo, Elaine R.;Massey, Dunecan;Blaszczyk, Kasia;Elliott, Timothy;Cotterill, Lynn;Dallal, Helen;Lobo, Alan J.;Mowat, Craig;Sanderson, Jeremy D.;Jewell, Derek P.;Newman, William G.;Edwards, Cathryn;Ahmad, Tariq;Mansfield, John C.;Satsangi, Jack;Parkes, Miles;Mathew, Christopher G.;Donnelly, Peter;Peltonen, Leena;Blackwell, Jenefer M.;Bramon, Elvira;Brown, Matthew A.;Casas, Juan P.;Corvin, Aiden;Craddock, Nicholas;Deloukas, Panos;Duncanson, Audrey;Jankowski, Janusz;Markus, Hugh S.;McCarthy, Mark I.;Palmer, Colin N. A.;Plomin, Robert;Rautanen, Anna;Sawcer, Stephen J.;Samani, Nilesh;Trembath, Richard C.;Viswanathan, Ananth C.;Wood, Nicholas;Spencer, Chris C. A.;Bellenguez, Celine;Davison, Daniel;Freeman, Colin;Strange, Amy;Langford, Cordelia;Hunt, Sarah E.;Edkins, Sarah;Gwilliam, Rhian;Blackburn, Hannah;Bumpstead, Suzannah J.;Dronov, Serge;Gillman, Matthew;Gray, Emma;Hammond, Naomi;Jayakumar, Alagurevathi;McCann, Owen T.;Liddle, Jennifer;Perez, Marc L.;Potter, Simon C.;Ravindrarajah, Radhi;Ricketts, Michelle;Waller, Matthew;Weston, Paul;Widaa, Sara;Whittaker, Pamela;Attwood, Antony P.;Stephens, Jonathan;Sambrook, Jennifer;Ouwehand, Willem H.;McArdle, Wendy L.;Ring, Susan M.;Strachan, David P.
通讯作者：
Strachan, David P.
影响因子：
4.4
作者：
Evans, Jamie G.;Chavez-Rueda, Karina A.;Mauri, Claudia
通讯作者：
Mauri, Claudia