Rajamuthiah Rajmohan, Mylonakis Eleftherios
a Division of Infectious Diseases; Rhode Island Hospital; Alpert Medical School of Brown University; Providence, RI USA.
Virulence. 2014;5(7):697-702. doi: 10.4161/viru.29091.
Pathogenic bacteria produce virulence factors called effectors, which are important components of the infection process. Effectors aid in pathogenesis by facilitating bacterial attachment, pathogen entry into or exit from the host cell, immunoevasion, and immunosuppression. Effectors also have the ability to subvert host cellular processes, such as hijacking cytoskeletal machinery or blocking protein translation. However, host cells possess an evolutionarily conserved innate immune response that can sense the pathogen through the activity of its effectors and mount a robust immune response. This "effector triggered immunity" (ETI) was first discovered in plants but recent evidence suggest that the process is also well conserved in metazoans. We will discuss salient points of the mechanism of ETI in metazoans from recent studies done in mammalian cells and invertebrate model hosts.
致病细菌会产生被称为效应蛋白的毒力因子,这些因子是感染过程的重要组成部分。效应蛋白通过促进细菌附着、病原体进入或离开宿主细胞、免疫逃避和免疫抑制来协助发病机制。效应蛋白还能够颠覆宿主细胞过程,例如劫持细胞骨架机制或阻断蛋白质翻译。然而,宿主细胞拥有一种进化上保守的先天免疫反应,该反应可以通过病原体效应蛋白的活性感知病原体并引发强烈的免疫反应。这种“效应蛋白触发免疫”(ETI)最早在植物中被发现,但最近的证据表明该过程在后生动物中也高度保守。我们将根据最近在哺乳动物细胞和无脊椎动物模型宿主中进行的研究,讨论后生动物中ETI机制的要点。