热休克蛋白70（Hsp70）可促进抗原呈递细胞的功能，并在体内将T细胞耐受性转变为自身免疫。

Hsp70 promotes antigen-presenting cell function and converts T-cell tolerance to autoimmunity in vivo.

作者信息

Millar Douglas G, Garza Kristine M, Odermatt Bernhard, Elford Alisha R, Ono Nobuyuki, Li Zihai, Ohashi Pamela S

机构信息

Departments of Immunology and Medical Biophysics, University Health Network, Ontario Cancer Institute, Toronto, Ontario M5G 2M9, Canada.

出版信息

Nat Med. 2003 Dec;9(12):1469-76. doi: 10.1038/nm962. Epub 2003 Nov 16.

DOI:10.1038/nm962

PMID:14625545

Abstract

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.

摘要

病原体或病原体相关分子模式可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，对于先天免疫系统如何检测组织损伤或坏死，我们了解得相对较少。有证据表明，热休克蛋白（HSPs）的释放可能提供类似佐剂的信号，但HSPs在体内促进激活或耐受的能力尚未得到研究。在本研究中，我们表明Hsp70可促进树突状细胞（DC）功能，并与抗原一起在体内引发自身免疫性疾病。