IgA adaptation to the presence of commensal bacteria in the intestine.
IgA adaptation to the presence of commensal bacteria in the intestine.
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DOI：
10.1007/3-540-30657-9_5
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发表时间：
2006
影响因子：
--
通讯作者：
A. Macpherson
中科院分区：
文献类型：
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作者：
A. Macpherson
哺乳动物的下肠由主要由非致病性肠道细菌组成的密集植物群定殖。这些肠道细菌对宿主的免疫和生理有广泛的影响。肠道定植后的一种适应是多特异性肠道伊加的产生和分泌增加。与对细菌定殖的强粘膜免疫应答相反，在无病原体的小鼠中，全身免疫系统仍然不知道这些生物体。少量细菌可以穿透覆盖派尔集合淋巴结的上皮表面并在树突状细胞中存活，以通过T依赖性和T非依赖性机制诱导伊加。这些负载有活的肠道生物体的树突状细胞可以归巢到肠系膜淋巴结，但不能到达全身的次级淋巴结构，因此粘膜反应的诱导集中在粘膜淋巴组织中。抗体在肠上皮表面的分泌反过来限制了肠道微生物的渗透，但这是使肠粘膜适应与肠道细菌共存的许多机制之一。
The lower intestine of mammals is colonised by a dense flora composed mainly of non-pathogenic commensal bacteria. These intestinal bacteria have a wide-ranging impact on host immunity and physiology. One adaptation following intestinal colonisation is increased production and secretion of polyspecific intestinal IgA. In contrast to the strong mucosal immune response to bacterial colonisation, the systemic immune system remains ignorant of these organisms in pathogen-free mice. Small numbers of bacteria can penetrate the epithelial surface overlying Peyer’s patches and survive in dendritic cells to induce IgA by T-dependent and T-independent mechanisms. These dendritic cells loaded with live commensal organisms can home to the mesenteric lymph nodes but do not reach systemic secondary lymphoid structures, so induction of mucosal responses is focused inmucosal lymphoid tissues. The secretion of antibodies across the intestinal epithelial surface in turn limits the penetration of commensal organisms, but this is one of many mechanisms which adapt the intestinal mucosa to co-existence with commensal bacteria.