A central role for inducible heat-shock protein 70 in autoimmune vitiligo.

A central role for inducible heat-shock protein 70 in autoimmune vitiligo.
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DOI:
10.1111/exd.12183
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发表时间:
2013-09
影响因子:
3.6
通讯作者:
Le Poole IC
Le Poole IC
中科院分区:
医学2区
文献类型:
--
作者:
Mosenson JA;Eby JM;Hernandez C;Le Poole IC

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诱导热休克蛋白70 (HSP70i)是一种受应激调节的保护细胞免于凋亡的蛋白。这些蛋白质在整个进化过程中都非常保守,这使得它们成为人们关注的焦点,因为它们有助于理解感染和免疫之间的有趣关系。在应激蛋白存在的情况下,树突状细胞(dc)会感知到这种警报信号,并通过招募不同羽毛的免疫细胞来适应这种情况。在紧张时期,黑素细胞会分泌抗原结合的HSP70i,作为激活dc的警报信号,dc具有起源地址,驱动白癜风的自身免疫反应。在这里,我们提出,如果自身免疫反应是通过HSP70i引导的,那么阻断应激蛋白激活dc可以为白癜风提供新的治疗机会。
Inducible Heat Shock Protein 70 (HSP70i) is a protein regulated by stress that protects cells from undergoing apoptosis. Such proteins are marvelously well conserved throughout evolution, which has placed them in the spotlight for helping to understand the intriguing relationship between infection and immunity. In the presence of stress proteins, dendritic cells (DCs) will sense this alarm signal and respond by recruiting immune cells of different plumage to fit the occasion. In times of stress, melanocytes will secrete antigen bound HSP70i to act as an alarm signal in activating DCs, that comes equipped with an address of origin to drive the autoimmune response in vitiligo. Here we pose that if the autoimmune response is funneled through HSP70i, then blocking the stress protein from activating DCs can lend new treatment opportunities for vitiligo.
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