炎症性肠病
发病机制
溃疡性结肠炎
疾病
免疫学
免疫病理学
病因学
炎症性肠病
免疫系统
医学
结肠炎
病理
作者
Yava Jones‐Hall,Matthew B. Grisham
出处
期刊:Pathophysiology
[Multidisciplinary Digital Publishing Institute]
日期:2014-05-27
卷期号:21 (4): 267-288
被引量:54
标识
DOI:10.1016/j.pathophys.2014.05.002
摘要
Inflammatory bowel diseases (IBD) are chronic, relapsing conditions of multifactorial etiology. The two primary diseases of IBD are Crohn's disease (CD) and ulcerative colitis (UC). Both entities are hypothesized to occur in genetically susceptible individuals due to microbial alterations and environmental contributions. The exact etiopathogenesis, however, is not known for either disease. A variety of mouse models of CD and UC have been developed to investigate the pathogenesis of these diseases and evaluate treatment modalities. Broadly speaking, the mouse models can be divided into 4 categories: genetically engineered, immune manipulated, spontaneous and erosive/chemically induced. No one mouse model completely recapitulates the immunopathology of CD or UC, however each model possesses particular similarities to human IBD and offers advantageous for specific details of IBD pathogenesis. Here we discuss the more commonly used models in each category and critically evaluate how the immunopathology induced compares to CD or UC, as well as the advantages and disadvantages associated with each model.
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