TLR1-induced chemokine production is critical for mucosal immunity against Yersinia enterocolitica.
TLR1-induced chemokine production is critical for mucosal immunity against Yersinia enterocolitica.
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我们的胃肠道是许多细菌和病毒的入口。因此，这种组织必须开发出快速诱导抗原特异性T细胞和抗体反应的方法。肠上皮细胞是屏障功能的核心参与者，也是将入侵病原体的信号传递到底层免疫组织的核心参与者。在这里，我们证明，Toll样受体1（TLR1）在上皮细胞的激活导致口腔感染小肠结肠炎耶尔森氏菌过程中的趋化因子CCL20的上调。此外，使用多克隆抗体处理中和CCL20和TLR1缺失均导致CCR6+树突状细胞（DC）的缺陷，所述树突状细胞产生有助于诱导抗耶尔森氏菌特异性T辅助17（TH17）细胞和伊加产生的先天性细胞因子。这些数据证明了TLR1信号传导在肠上皮中的新作用，并证明TLR1和CCL20一起通过DC的活化和募集是TH17免疫的关键介质。
Our gastrointestinal tract is a portal of entry for a number of bacteria and viruses. Thus, this tissue must develop ways to induce antigen-specific T cell and antibody responses quickly. Intestinal epithelial cells are a central player in barrier function and also in communicating signals from invading pathogens to the underlying immune tissue. Here we demonstrate that activation of Toll-like receptor 1 (TLR1) in the epithelium leads to the upregulation of the chemokine CCL20 during oral infection with Yersinia enterocolitica. Further, both neutralization of CCL20 using polyclonal antibody treatment and deletion of TLR1 resulted in a defect in CCR6+ dendritic cells (DCs), which produce innate cytokines that help to induce anti-Yersinia-specific T helper 17 (TH17) cells and IgA production. These data demonstrate a novel role for TLR1 signaling in the intestinal epithelium and demonstrate that together TLR1 and CCL20 are critical mediators of TH17 immunity through the activation and recruitment of DCs.
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影响因子：
3.8
作者：
KHORAMIANFALSAFI, T;HARAYAMA, S;PECHERE, JC
通讯作者：
PECHERE, JC
影响因子：
4.4
作者：
Johnson, Christopher M.;Lyle, Elizabeth A.;Tapping, Richard I.
通讯作者：
Tapping, Richard I.
影响因子：
30.3
作者：
DePaolo, R. William;Tang, Fangming;Jabri, Bana
通讯作者：
Jabri, Bana
影响因子：
32.4
作者：
Kang, Jin Young;Nan, Xuehua;Lee, Jie-Oh
通讯作者：
Lee, Jie-Oh
DOI：
10.1152/ajpgi.2001.280.4.g710
发表时间：
2001-04-01
影响因子：
4.5
作者：
Izadpanah, A;Dwinell, MB;Kagnoff, MF
通讯作者：
Kagnoff, MF