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.

中文翻译：

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巨噬细胞在对弓形虫的保护和病理反应中的作用。

的能力弓形虫引起临床疾病中再加上其易用性在免疫感受态和免疫缺陷的宿主体外和小鼠模型的可用性，导致了其作为模式生物研究使用如何免疫系统控制的细胞内感染。本文回顾了建立细胞因子IFN-γ在激活巨噬细胞以控制弓形虫中的作用的研究以及导致动员和扩展巨噬细胞种群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，并具有促进炎症消退的调节特性。然而，尽管巨噬细胞在确定感染的结果中很重要，但刚地弓形虫已经进化出破坏巨噬细胞活化的机制，并可以利用其迁移活动促进传播，而这两个特性是该寄生虫持久并引起疾病的能力的基础。