Entomopathogenic fungi (EPF) have been widely explored for their potential in the biological control of insect pests and as an environmentally friendly alternative to acaricides for limiting tick infestation in the field. The arthropod cuticle is the main barrier against fungal infection, however, an understanding of internal defense mechanisms after EPF intrusion into the invertebrate hemocoel is still rather limited. Using an infection model of the European Lyme borreliosis vector Ixodes ricinus with the EPF Metarhizium robertsii, we demonstrated that ticks are capable of protecting themselves to a certain extent against mild fungal infections. However, tick mortality dramatically increases when the capability of tick hemocytes to phagocytose fungal conidia is impaired. Using RNAi-mediated silencing of tick thioester-containing proteins (TEPs), followed by in vitro and/or in vivo phagocytic assays, we found that C3-like complement components and α2-macroglobulin pan-protease inhibitors secreted to the hemolymph play pivotal roles in M. robertsii phagocytosis.

昆虫病原真菌 (EPF) 已被广泛探索，因为它们在生物防治害虫方面的潜力以及作为一种环境友好的杀螨剂替代品来限制田间蜱虫的侵扰。节肢动物的角质层是抵抗真菌感染的主要屏障，然而，对 EPF 侵入无脊椎动物血腔后的内部防御机制的了解仍然相当有限。使用欧洲莱姆疏螺旋体病载体Ixodes ricinus与 EPF Metarhizium robertsii的感染模型，我们证明了蜱能够在一定程度上保护自己免受轻度真菌感染。然而，当蜱血细胞吞噬真菌分生孢子的能力受损时，蜱死亡率会显着增加。使用 RNAi 介导的含蜱硫酯蛋白 (TEP) 的沉默，然后进行体外和/或体内吞噬测定，我们发现分泌到血淋巴的 C3 样补体成分和 α2-巨球蛋白泛蛋白酶抑制剂起着关键作用在M. robertsii吞噬作用中。