University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, USA.
Kangwon National University College of Veterinary Medicine and Institute of Veterinary Science, Chuncheon, Korea.
Parasite Immunol. 2020 Jul;42(7):e12712. doi: 10.1111/pim.12712. Epub 2020 Apr 8.
The ability of Toxoplasma gondii to cause clinical disease in immune-competent and immune-deficient hosts coupled with its ease of use in vitro and availability of murine models has led to its use as a model organism to study how the immune system controls an intracellular infection. This article reviews the studies that established the role of the cytokine IFN-γ in the activation of macrophages to control T gondii and the events that lead to the mobilization and expansion of macrophage populations and their ability to limit parasite replication. Macrophages also have pro-inflammatory functions that promote protective NK and T-cell activities as well as regulatory properties that facilitate the resolution of inflammation. Nevertheless, while macrophages are important in determining the outcome of infection, T gondii has evolved mechanisms to subvert macrophage activation and can utilize their migratory activities to promote dissemination and these two properties underlie the ability of this parasite to persist and cause disease.
刚地弓形虫能够在免疫功能正常和免疫功能低下的宿主中引起临床疾病,加上其易于在体外使用和具有鼠类模型,使其成为研究免疫系统如何控制细胞内感染的模型生物。本文综述了研究确立细胞因子 IFN-γ在激活巨噬细胞以控制刚地弓形虫中的作用,以及导致巨噬细胞群体动员和扩增及其限制寄生虫复制能力的事件。巨噬细胞还具有促炎功能,可促进保护性 NK 和 T 细胞活性,以及调节特性,可促进炎症消退。然而,虽然巨噬细胞在确定感染结局方面很重要,但刚地弓形虫已进化出抑制巨噬细胞激活的机制,并可利用其迁移活动促进传播,这两个特性是该寄生虫持续存在和引起疾病的基础。