Immune responses of TLR5+ lamina propria dendritic cells in enterobacterial infection

被引:0
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作者
Satoshi Uematsu
Shizuo Akira
机构
[1] Osaka University,Laboratory of Host Defense, WPI Immunology Frontier Research Center
[2] Osaka University,Department of Host Defense, Research Institute for Microbial Diseases
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关键词
Lamina propria; TLR5; IgA; Th17; Autophagy;
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摘要
Toll-like receptors (TLRs) recognize distinct microbial components and induce innate immune responses. TLR5 has been shown to recognize bacterial flagellin. Unlike other TLRs, TLR5 is not expressed on conventional dendritic cells or macrophages. By contrast, TLR5 is mainly expressed on intestinal CD11c+ lamina propria cells (LPCs), which do not express TLR4. These cells detect pathogenic bacteria and secreted proinflammatory cytokines, mainly in a TLR5-dependent manner. Notably, transport of pathogenic Salmonella typhimurium from the intestinal tract to mesenteric lymph nodes was impaired in Tlr5−/− mice, suggesting that CD11c+ LPCs expressing TLR5 are used by S. typhimurium for systemic infection. CD11c+ LPCs consist of four subsets distinguished by differential expression patterns of CD11c and CD11b. CD11chiCD11bhi LPDCs have been identified as TLR5-expressing cells. In response to flagellin, these LPDCs induce the differentiation of naive B cells into IgA+ plasma cells via a mechanism independent of gut-associated lymphoid tissue (GALT), and trigger the differentiation of antigen-specific Th17 and Th1 cells. These LPDCs have unique properties in that they can induce acquired immunity as well as innate immunity via TLR5 in the intestine.
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页码:803 / 811
页数:8
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