小鼠肠道菌群引入后的黏膜免疫反应及克隆氏病小鼠模型的建立

S. Matsumoto
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引用次数: 2

摘要

肠道菌群在肠黏膜免疫系统的成熟过程中发挥着关键作用,如肠上皮细胞上ⅱ类MHC抗原的表达,以及小鼠肠固有层中产生iga的B淋巴细胞和肠上皮中表达TCR的上皮内淋巴细胞的细胞扩增和功能成熟。在正常小鼠中,通过肠道菌群定植引起的粘膜免疫反应达到了在正常肠道菌群条件下饲养的小鼠的水平。然而,在SAMP1/Yit小鼠(最近建立的克罗恩病小鼠模型)中,尽管在无菌条件下未观察到肠道炎症,但在正常小鼠引入共生肠道菌群后,发生了跨壁回肠炎和盲肠炎。这些结果表明,在SAMP1/ Yit小鼠中,共生肠道菌群在克罗恩病样肠道炎症的发展中起关键作用。在这篇综述中,我们关注肠道菌群和粘膜免疫系统之间的特定相互作用,诱导生理性或非生理性粘膜免疫反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mucosal Immune Responses to the Introduction of Gut Flora in Mice and the Establishment of a Murine Model of Crohn's Disease
Gut flora plays a key role in the maturation of intestinal mucosal immune systems such as the expression of class II MHC antigens on intestinal epithelial cells, and the cell expansion and functional maturation of both IgA-producing B lymphocytes in the lamina propria and TCR expressing intraepithelial lymphocytes in the intestinal epithelium in mice. In normal mice, the mucosal immune responses evoked through colonization of gut flora attained levels found in mice reared under normal gut flora-bearing conditions. However, in SAMP1/Yit mice, recently established as a murine model of Crohn's disease, transmural ileitis and cecetis developed following the introduction of commensal gut flora from normal mice, although no intestinal inflammation was observed under germfree conditions. These results suggested that commensal gut flora play critical roles in the development of Crohn's disease-like intestinal inflammation in SAMP1/ Yit mice. In this review, we focus on the specific interactions between the gut flora and mucosal immune systems that induce physiological or unphysiological mucosal immune responses.
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