20-羟基蜕皮酮调控昆虫先天免疫的分子机制研究进展

Progress in the molecular mechanisms underlying the regulation of innate immunity by 20-hydroxyecdysone in insects

昆虫先天免疫(innate immunity)包括细胞免疫(cellular immunity)和体液免疫(humoral immunity)。近年来研究表明,作为昆虫生长发育调节的关键激素之一,20-羟基蜕皮酮(20-hydroxyecdysone, 20E)参与调节了昆虫的先天免疫。本文在介绍昆虫免疫机制的基础上,重点阐述20E调控昆虫先天免疫及微生物影响20E滴度的分子调控机制。20E可以激活细胞免疫和体液免疫来对抗外源入侵微生物,而外源微生物的刺激也会通过3-脱氢蜕皮激素-3β-还原酶(3-dehydroecdysteroid-3β-reductase, 3DE-3β-reductase)促进20E滴度升高。20E对昆虫免疫系统有显著影响,其滴度升高可以激活细胞免疫,包括吞噬(phagocytosis)、包被(encapsulation)和结节(nodulation);而对体液免疫的影响则比较复杂,除可以加速黑化作用(menalization)外,对抗菌肽的表达究竟是促进还是抑制尚不明确。研究人员鉴定发现了一些20E调控体液免疫的关键基因,这些基因的作用途径总结起来可以分为3类:(1)依赖于Toll和IMD等先天免疫通路;(2)依赖于胰岛素(insulin)信号途径;(3)依赖于20E信号通路因子BR-C等的直接调控。但这些通路因子究竟是如何互作以及其分子调控机制等都尚不清楚,值得进一步深入探讨。

The innate immunity of insects includes cellular immunity and hurmoral immunity. Recent studies have shown that 20-hydroxyecdysone （20E）, one of the key hormones in the regulation of insect growth and development, is involved in the regulation of insect innate immunity. In this article we focus on the molecular mechanisms of 20E regulating the innate immunity in insects and the influence of microorganisms on 20E titer based on the mechanisms of insect immunity. 20E can activate cellular and humoral immunity against invasive microorganisms, and the stimulation of exogenous microorganisms can promote the increase of 20E titer by 3-dehydroecdysteroid-3β-reductase （3DE-3β-reductase）. 20E has a significant effect on the immune system of insects, and the increase of its titer can activate cellular immunity, including phagocytosis, encapsulation and nodulation, while the effect on humoral immunity is more complex. Besides accelerating melanization, whether 20E promotes or inhibits the expression of antimicrobial peptides is not clear yet. Researchers identified a number of key genes through which 20E regulates humoral immunity, and they can be grouped into three categories according to the pathways they are involved in： the first is dependent on innate immune pathways such as Toll and IMD, the second is dependent on insulin signaling pathways, and the third is the direct regulation by 20E signaling pathway via such transcription factors as BR-C. However, the way these pathway factors interact with each other and their molecular regulatory mechanisms are still unclear and deserve further study.