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Toll-like receptor激动剂耐受分子机制和疟原虫慢性感染 被引量:2

The molecule basis of Toll-like receptor agonist-induced tolerance and its role in malaria parasite chronic infection
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摘要 小剂量LPS预刺激可引起内毒素耐受,能提高小鼠在致死剂量LPS再次刺激后的存活率,其机制可能与铎样受体TLR(Toll-like receptor)4信号通路的下调有关。近年来的研究发现,其他TLR激动剂同样可以引起宿主对相应TLR激动剂和LPS的耐受,后者称为交叉耐受(cross tolerance),而且疟原虫慢性感染同样能诱导类似TLR激动剂耐受的现象,因此,研究TLR激动剂耐受分子机制有助于脓毒血症预防和对慢性感染机制的理解。 Pre-exposure of low-dose LPS confers host hyposensitivity to secondary LPS stimulation, which is known as endotoxin tolerance. Evidence showed endotoxin tolerance is associated with down-regulation of Toll-like receptor 4 (TLR 4) signaling pathway. In recent years, pre-exposure of other TLRs agonists were also reported to confer host tolerance to themselves as well as LPS, and the latter was called cross-tolerance. In addition, infection of malaria parasites could also induce DC into tolerance status. Hence, exploring the molecular basis of tolerance will provide us novel targets to prevent sepsis, and help us to understand the mechanism of chronic infection diseases.
出处 《免疫学杂志》 CAS CSCD 北大核心 2008年第5期595-598,600,共5页 Immunological Journal
基金 国家自然科学基金项目(30771877)
关键词 铎样受体激动剂 脓毒血症 耐受 疟原虫 Toll-like receptor agonist Sepsis Tolerance Malaria parasites
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