Hsp70 promotes antigen-presenting cell function and converts T-cell tolerance to autoimmunity in vivo
Hsp70 promotes antigen-presenting cell function and converts T-cell tolerance to autoimmunity in vivo
复制标题
DOI：
10.1038/nm962
复制
发表时间：
2003-12-01
期刊：
影响因子：
82.9
通讯作者：
Ohashi, PS
中科院分区：
文献类型：
--
作者：
Millar, DG;Garza, KM;Ohashi, PS
病原体或病原体相关的分子模式可以向先天免疫系统的细胞发出信号并触发有效的适应性免疫。然而，关于先天免疫系统如何检测组织损伤或坏死的知识相对较少。有证据表明，热休克蛋白（HSP）的释放可能提供佐剂样信号，但HSP在体内促进活化或耐受的能力尚未得到解决。在这项研究中，我们表明，热休克蛋白70促进树突状细胞（DC）的功能，并与抗原一起，触发体内自身免疫性疾病。
Pathogens or pathogen- associated molecular patterns can signal to cells of the innate immune system and trigger effective adaptive immunity. However, relatively little is known about how the innate immune system detects tissue injury or necrosis. Evidence suggests that the release of heat- shock proteins (HSPs) may provide adjuvant- like signals, but the ability of HSPs to promote activation or tolerance in vivo has not been addressed. In this study we show that Hsp70 promotes dendritic cell (DC) function and, together with antigen, triggers autoimmune disease in vivo.