生物谷报道：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 J Ishii1,10,11 & Shizuo Akira1,2,10
Abstract
The intestinal cell types responsible for defense against pathogenic organisms remain incompletely characterized. Here we identify a subset of CD11chiCD11bhi 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.
Laboratory of Host Defense, Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
Laboratory of Gastrointestinal Immunology, Immunology Frontier Research Center, Osaka University, Suita, Osaka 565-0871, Japan.
Department of Microbiology, Gachon Medical School, Incheon 405-760, Korea.
Laboratory of Immunodynamics, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan.
Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, University of Tokyo, 108-8639 Tokyo, Japan.
Department of Pathology, Hyogo College of Medicine, 1, Mukogawa, Nishinomiya, Hyogo 663-8501, Japan.
Department of Microbiology and Immunology, Nihon University School of Dentistry at Matsudo, Chiba 271-8587, Japan.
Division of Molecular Genetics, School of Medicine, Faculty of Medical Sciences, University of Fukui, Fukui 910-1193, Japan.
Exploratory Research for Advanced Technology, Japan Science and Technology Corporation, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
Department of Molecular Protozoology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
These authors contributed equally to this work.
Correspondence to: Shizuo Akira1,2,10 e-mail: sakira@biken.osaka-u.ac.jp
