Infection and Innate Immunity Lab, Department of Biological Sciences, The George Washington University, Washington, DC 20052, USA.
Int J Mol Sci. 2024 Jul 21;25(14):7970. doi: 10.3390/ijms25147970.
Despite impressive advances in the broad field of innate immunity, our understanding of the molecules and signaling pathways that control the host immune response to nematode infection remains incomplete. We have shown recently that Transforming Growth Factor-β (TGF-β) signaling in the fruit fly is activated by nematode infection and certain TGF-β superfamily members regulate the anti-nematode immune response. Here, we investigate the effect of an entomopathogenic nematode infection factor on host TGF-β pathway regulation and immune function. We find that serine carboxypeptidase activates the Activin branch in adults and the immune deficiency pathway in Activin-deficient flies, it affects hemocyte numbers and survival in flies deficient for Activin signaling, and causes increased intestinal steatosis in Activin-deficient flies. Thus, insights into the signaling pathways and metabolic processes interacting with pathogenicity factors will be applicable to entomopathogenic nematode infection of important agricultural insect pests and vectors of disease.
尽管在先天免疫这一广阔领域取得了令人瞩目的进展，但我们对于控制宿主对寄生虫感染的免疫反应的分子和信号通路的理解仍不完整。我们最近表明，在果蝇中，转化生长因子-β（TGF-β）信号被寄生虫感染激活，某些 TGF-β超家族成员调节抗寄生虫免疫反应。在这里，我们研究了一种昆虫病原线虫感染因子对宿主 TGF-β 途径调节和免疫功能的影响。我们发现丝氨酸羧肽酶在成虫中激活激活素分支，在 Activin 缺陷型果蝇中激活免疫缺陷途径，它影响 Activin 信号缺陷型果蝇的血细胞数量和存活，并导致 Activin 缺陷型果蝇的肠道脂肪变性增加。因此，与致病性因子相互作用的信号通路和代谢过程的见解将适用于重要农业害虫和疾病传播媒介的昆虫病原线虫感染。
