Garg Ravendra, Trudel Nathalie, Tremblay Michel J
Centre de Recherche en Infectiologie, Centre Hospitalier de l'Université Laval, 2705 Boulevard Laurier, RC-709, Université Laval, Québec, G1V 4G2, Canada.
Trends Parasitol. 2007 Jul;23(7):317-24. doi: 10.1016/j.pt.2007.05.006. Epub 2007 May 24.
Recent studies have shown that both Leishmania and HIV type-1 (HIV-1) hijack dendritic cell (DC) functions to escape immune surveillance using an array of elaborate strategies. Leishmania has developed a variety of adaptations to disrupt cellular defense mechanisms, whereas HIV-1 targets DCs to achieve a more efficient dissemination. The capacity of Leishmania and HIV-1 to target DCs through a common cell-surface molecule, namely DC-SIGN (dendritic cell specific ICAM-3-grabbing non-integrin), points to a possible dangerous liaison between these two pathogens. This review explores our knowledge of how Leishmania and HIV-1 interact dynamically with DCs, and how they exploit this cell type for their reciprocal benefit.
最近的研究表明,利什曼原虫和1型人类免疫缺陷病毒(HIV-1)都利用一系列复杂的策略劫持树突状细胞(DC)的功能以逃避免疫监视。利什曼原虫已形成多种适应性变化来破坏细胞防御机制,而HIV-1则以DC为靶点以实现更有效的传播。利什曼原虫和HIV-1通过一种共同的细胞表面分子,即DC-SIGN(树突状细胞特异性细胞间黏附分子3抓取非整合素)靶向DC的能力,表明这两种病原体之间可能存在危险的关联。这篇综述探讨了我们对于利什曼原虫和HIV-1如何与DC动态相互作用,以及它们如何利用这种细胞类型实现互利的了解。