Downstream effector functions of T-cell activation.
Downstream effector functions of T-cell activation.
复制标题
T 细胞激活的下游效应器功能。
DOI：
10.1097/00005176-200504001-00014
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发表时间：
2005
影响因子：
2.9
通讯作者：
Strober,Warren
中科院分区：
文献类型：
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作者：
Strober,Warren
从对炎症性肠病(IBD)小鼠模型的研究中得出的主要见解之一是，在迄今已报道的无数模型中发展起来的炎症可以归因于最终的共同途径，该途径使用Th1或Th2效应细胞作为炎症的驱动力。此外，这两类模型在组织学上分别类似于IBD的两种主要形式，克罗恩病(CD)和溃疡性结肠炎(UC)。两种直肠内安装TNBS和恶唑酮后的粘膜炎症诱导模型说明了这一点。SJL/J或C57BL/10小鼠的TNBS结肠炎是一种Th1介导的炎症，以高IL-12和高干扰素产生为特征，并通过给予抗IL-12(Antip40)抗体来预防和治疗。事实上，正是这种观察直接导致了在人类CD患者中进行抗IL-12治疗的试验，表明该抗体诱导了Th1反应的改善和良好的临床反应。这些对患者的研究构成了CD实际上是由Th1效应细胞驱动的炎症所致的正式证据。
One of the major insights to emerge from the study of mouse models of inflammatory bowel disease (IBD) is that the inflammation that develops in the myriad of models so far reported can be assigned to a final common pathway that uses either a Th1 or a Th2 effector cell as the driving force of the inflammation. Moreover, these two classes of models resemble histologically the two major forms of IBD, Crohn’s disease (CD) and ulcerative colitis (UC), respectively.Two of the “induced” models of mucosal inflammation that follow intra-rectal installation of TNBS and oxazolone illustrate this point. TNBS-colitis in SJL/J or C57Bl/10 mice is a Th1-mediated inflammation characterized by high IL-12 and IFN-production and is prevented and treated by administration of anti-IL-12 (antip40) antibody. It was in fact this observation that led directly to a trial of anti-IL-12 treatment in human CD patients that showed that the antibody induced an amelioration of the Th1 response and an excellent clinical response. These studies in patients constitute a formal proof that CD is in fact due to a Th1 effector cell-driven inflammation.