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溃疡性结肠炎的细胞与分子免疫发病机制

Cellular and molecular immunopathogenesis of ulcerative colitis.

作者信息

Zhang Su Zhen, Zhao Xu Hui, Zhang De Chun

机构信息

Department of Laboratory Medicine, Chongqing University of Medical Science, China.

出版信息

Cell Mol Immunol. 2006 Feb;3(1):35-40.

Abstract

Ulcerative colitis (UC) is an inflammatory disease of the rectal and colonic mucosa and seems to result from a complex series of interactions between susceptibility genes, the environment and the immune system. Various components of the mucosal immune system are implicated in the immunopathogenesis of UC. Evidence from animal models also suggests that an altered immune response to the commensal microflora of the host plays a central role in the development of UC. So in this review, we elucidate the cells and molecules which are implicated in the immunopathogenesis of the disease from four aspects: antigens in the intestine, dendritic cells, toll like receptors and NF-kappaB in the UC.

摘要

溃疡性结肠炎(UC)是一种直肠和结肠黏膜的炎症性疾病,似乎是由易感基因、环境和免疫系统之间一系列复杂的相互作用导致的。黏膜免疫系统的各种成分都与UC的免疫发病机制有关。动物模型的证据也表明,宿主对共生微生物群的免疫反应改变在UC的发展中起核心作用。因此,在本综述中,我们从四个方面阐明了与该疾病免疫发病机制相关的细胞和分子:肠道中的抗原、树突状细胞、Toll样受体以及UC中的核因子κB。

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