Nature Immun：日专家发现抵御肠道病原菌的新免疫细胞 - 生物研究-生物谷

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日本大阪大学的研究人员在新一期英国《自然·免疫学》杂志上报告说，他们发现小肠黏膜内存在一种免疫细胞，该细胞能监视病原菌是否企图通过小肠黏膜“深度侵犯”人体，并催生可合成抗体以抵御病原菌的细胞。

大阪大学教授审良静男领导的小组发现了一种名为“ＬＰＤＣ”的

树突状细胞，它在小肠黏膜中发挥作用。肠道内的病原菌如果企图通过小肠黏膜，进入人体组织和血液循环，“ＬＰＤＣ”细胞表面分泌的蛋白质“ＴＬＲ５”就能产生感应，从而启动攻击病原菌的免疫系统。“ＬＰＤＣ”细胞会催生另一种细胞，后者能分泌抵抗病原菌的抗体。

在深入研究中，研究人员发现“ＬＰＤＣ”细胞还与辅助性Ｔ细胞中的“Ｔｈ１”和“Ｔｈ１７”细胞的生成密切相关，而辅助性Ｔ细胞是发布攻击病原菌命令的“司令部”。

在此前相当长的时间里，很多研究者认为只有淋巴组织中的免疫细胞才能产生抗体。但近些年，专家们在没有淋巴组织的小鼠体内同样发现了抗体，探究该现象机制的工作正在展开。（生物谷援引新华网）

生物谷推荐原始出处：

Nature Immunology
Published online: 30 May 2008 | doi:10.1038/ni.1622

Regulation of humoral and cellular gut immunity by lamina propria dendritic cells expressing Toll-like receptor 5

Satoshi Uematsu1,2,12,Kosuke Fujimoto1,2,12, Myoung Ho Jang3, Bo-Gie Yang1, Yun-Jae Jung4,Mika Nishiyama5, Shintaro Sato6, Tohru Tsujimura7, Masafumi Yamamoto8,Yoshifumi Yokota9, Hiroshi Kiyono6, Masayuki Miyasaka5, Ken JIshii1,10,11 & Shizuo Akira1,2,10

The intestinal cell typesresponsible for defense against pathogenic organisms remain incompletelycharacterized. Here we identify a subset of CD11chiCD11bhi laminapropria dendritic cells (LPDCs) that expressed Toll-like receptor 5(TLR5) in the small intestine. When stimulated by the TLR5 ligandflagellin, TLR5+ LPDCs induced the differentiation of naive B cells intoimmunoglobulin A–producing plasma cells by a mechanism independent ofgut-associated lymphoid tissue. In addition, by a mechanism dependent onTLR5 stimulation, these LPDCs promoted the differentiation ofantigen-specific interleukin 17–producing T helper cells and type 1 Thelper cells. Unlike spleen DCs, the LPDCs specifically producedretinoic acid, which, in a dose-dependent way, supported the generationand retention of immunoglobulin A–producing cells in the lamina propriaand positively regulated the differentiation interleukin 17–producing Thelper cells. Our findings demonstrate unique properties of LPDCs andthe importance of TLR5 for adaptive immunity in the intestine.

  1. Laboratory of Host Defense, Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
  2. Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
  3. Laboratory of Gastrointestinal Immunology, Immunology Frontier Research Center, Osaka University, Suita, Osaka 565-0871, Japan.
  4. Department of Microbiology, Gachon Medical School, Incheon 405-760, Korea.
  5. Laboratory of Immunodynamics, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan.
  6. Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, University of Tokyo, 108-8639 Tokyo, Japan.
  7. Department of Pathology, Hyogo College of Medicine, 1, Mukogawa, Nishinomiya, Hyogo 663-8501, Japan.
  8. Department of Microbiology and Immunology, Nihon University School of Dentistry at Matsudo, Chiba 271-8587, Japan.
  9. Division of Molecular Genetics, School of Medicine, Faculty of Medical Sciences, University of Fukui, Fukui 910-1193, Japan.
  10. Exploratory Research for Advanced Technology, Japan Science and Technology Corporation, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
  11. Department of Molecular Protozoology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
  12. These authors contributed equally to this work.

Correspondence to: Shizuo Akira1,2,10 e-mail: sakira@biken.osaka-u.ac.jp