生物谷報(bào)道：日本大阪大學(xué)的研究人員在新一期英國(guó)《自然·免疫學(xué)》雜志上報(bào)告說(shuō),，他們發(fā)現(xiàn)小腸黏膜內(nèi)存在一種免疫細(xì)胞，該細(xì)胞能監(jiān)視病原菌是否企圖通過(guò)小腸黏膜“深度侵犯”人體,，并催生可合成抗體以抵御病原菌的細(xì)胞,。
大阪大學(xué)教授審良靜男領(lǐng)導(dǎo)的小組發(fā)現(xiàn)了一種名為“ＬＰＤＣ”的
樹突狀細(xì)胞，它在小腸黏膜中發(fā)揮作用,。腸道內(nèi)的病原菌如果企圖通過(guò)小腸黏膜,，進(jìn)入人體組織和血液循環(huán)，“ＬＰＤＣ”細(xì)胞表面分泌的蛋白質(zhì)“ＴＬＲ５”就能產(chǎn)生感應(yīng)，從而啟動(dòng)攻擊病原菌的免疫系統(tǒng),。“ＬＰＤＣ”細(xì)胞會(huì)催生另一種細(xì)胞,，后者能分泌抵抗病原菌的抗體。
在深入研究中,，研究人員發(fā)現(xiàn)“ＬＰＤＣ”細(xì)胞還與輔助性Ｔ細(xì)胞中的“Ｔｈ１”和“Ｔｈ１７”細(xì)胞的生成密切相關(guān),，而輔助性Ｔ細(xì)胞是發(fā)布攻擊病原菌命令的“司令部”。
在此前相當(dāng)長(zhǎng)的時(shí)間里,，很多研究者認(rèn)為只有淋巴組織中的免疫細(xì)胞才能產(chǎn)生抗體,。但近些年，專家們?cè)跊](méi)有淋巴組織的小鼠體內(nèi)同樣發(fā)現(xiàn)了抗體,，探究該現(xiàn)象機(jī)制的工作正在展開,。（生物谷援引新華網(wǎng)）
生物谷推薦原始出處：
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: [email protected]
