Regulation of humoral and cellular gut immunity by lamina propria dendritic cells expressing Toll-like receptor 5
Regulation of humoral and cellular gut immunity by lamina propria dendritic cells expressing Toll-like receptor 5
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DOI：
10.1038/ni.1622
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发表时间：
2008-07-01
影响因子：
30.5
通讯作者：
Akira, Shizuo
中科院分区：
文献类型：
--
作者：
Uematsu, Satoshi;Fujimoto, Kosuke;Akira, Shizuo
负责防御病原生物的肠道细胞类型仍未完全确定。在这里，我们鉴定了在小肠中表达toll样受体5 （TLR5）的CD11c(hi)CD11b（hi）固有层树突状细胞（LPDCs）的一个亚群。在TLR5配体鞭毛蛋白的刺激下，TLR5(+) LPDCs通过独立于肠道相关淋巴组织的机制诱导幼稚B细胞分化为产生免疫球蛋白a的浆细胞。此外，通过依赖于TLR5刺激的机制，这些LPDCs促进了抗原特异性产生白细胞介素17的T辅助细胞和1型T辅助细胞的分化。与脾dc不同，LPDCs特异性产生维甲酸，以剂量依赖的方式支持固有层中产生免疫球蛋白a的细胞的产生和保留，并积极调节产生白细胞介素17的T辅助细胞的分化。我们的研究结果证明了LPDCs的独特特性以及TLR5对肠道适应性免疫的重要性。
The intestinal cell types responsible for defense against pathogenic organisms remain incompletely characterized. Here we identify a subset of CD11c(hi)CD11b(hi) lamina propria dendritic cells (LPDCs) that expressed Toll-like receptor 5 (TLR5) in the small intestine. When stimulated by the TLR5 ligand flagellin, TLR5(+) LPDCs induced the differentiation of naive B cells into immunoglobulin A-producing plasma cells by a mechanism independent of gut-associated lymphoid tissue. In addition, by a mechanism dependent on TLR5 stimulation, these LPDCs promoted the differentiation of antigen-specific interleukin 17-producing T helper cells and type 1 T helper cells. Unlike spleen DCs, the LPDCs specifically produced retinoic acid, which, in a dose-dependent way, supported the generation and retention of immunoglobulin A-producing cells in the lamina propria and positively regulated the differentiation interleukin 17-producing T helper cells. Our findings demonstrate unique properties of LPDCs and the importance of TLR5 for adaptive immunity in the intestine.