Elson Charles O, Cong Yingzi, McCracken Vance J, Dimmitt Reed A, Lorenz Robin G, Weaver Casey T
Division of Gastroenterology and Hepatology, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294-0007, USA.
Immunol Rev. 2005 Aug;206:260-76. doi: 10.1111/j.0105-2896.2005.00291.x.
There are now many experimental models of inflammatory bowel disease (IBD), most of which are due to induced mutations in mice that result in an impaired homeostasis with the intestinal microbiota. These models can be clustered into several broad categories that, in turn, define the crucial cellular and molecular mechanisms of host microbial interactions in the intestine. The first of these components is innate immunity defined broadly to include both myeloid and epithelial cell mechanisms. A second component is the effector response of the adaptive immune system, which, in most instances, comprises the CD4+ T cell and its relevant cytokines. The third component is regulation, which can involve multiple cell types, but again particularly involves CD4+ T cells. Severe impairment of a single component can result in disease, but many models demonstrate milder defects in more than one component. The same is true for both spontaneous models of IBD, C3H/HeJBir and SAMPI/Yit mice. The thesis is advanced that 'multiple hits' or defects in these interacting components is required for IBD to occur in both mouse and human.
目前有许多炎症性肠病（IBD）的实验模型，其中大多数是由于小鼠中的诱导突变导致肠道微生物群稳态受损。这些模型可分为几大类，进而定义了宿主与肠道微生物相互作用的关键细胞和分子机制。这些组成部分中的第一个是广义上定义的固有免疫，包括髓样细胞和上皮细胞机制。第二个组成部分是适应性免疫系统的效应反应，在大多数情况下，包括CD4+T细胞及其相关细胞因子。第三个组成部分是调节，它可能涉及多种细胞类型，但同样特别涉及CD4+T细胞。单个组成部分的严重受损可导致疾病，但许多模型显示不止一个组成部分存在较轻的缺陷。IBD的自发模型C3H/HeJBir和SAMPI/Yit小鼠也是如此。有人提出这样的论点，即在小鼠和人类中发生IBD都需要这些相互作用的组成部分出现“多重打击”或缺陷。
