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首页> 外文期刊>Infection and immunity >Migratory Activation of Primary Cortical Microglia upon Infection with Toxoplasma gondii
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Migratory Activation of Primary Cortical Microglia upon Infection with Toxoplasma gondii

机译：弓形虫感染后原代皮层小胶质细胞的迁移活化

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Disseminated toxoplasmosis in the central nervous system (CNS) is often accompanied by a lethal outcome. Studies with murine models of infection have focused on the role of systemic immunity in control of toxoplasmic encephalitis, while knowledge remains limited on the contributions of resident cells with immune functions in the CNS. In this study, the role of glial cells was addressed in the setting of recrudescent Toxoplasma infection in mice. Activated astrocytes and microglia were observed in the close vicinity of foci with replicating parasites in situ in the brain parenchyma. Toxoplasma gondii tachyzoites were allowed to infect primary microglia and astrocytes in vitro. Microglia were permissive to parasite replication, and infected microglia readily transmigrated across transwell membranes and cell monolayers. Thus, infected microglia, but not astrocytes, exhibited a hypermotility phenotype reminiscent of that recently described for infected dendritic cells. In contrast to gamma interferon-activated microglia, Toxoplasma-infected microglia did not upregulate major histocompatibility complex (MHC) class II molecules and the costimulatory molecule CD86. Yet Toxoplasma-infected microglia and astrocytes exhibited increased sensitivity to T cell-mediated killing, leading to rapid parasite transfer to effector T cells in vitro. We hypothesize that glial cells and T cells, besides their role in triggering antiparasite immunity, may also act as “Trojan horses,” paradoxically facilitating dissemination of Toxoplasma within the CNS. To our knowledge, this constitutes the first report of migratory activation of a resident CNS cell by an intracellular parasite.
机译：中枢神经系统（CNS）中传播的弓形虫病通常伴随致命的后果。关于鼠类感染模型的研究集中于全身免疫在控制弓形虫性脑炎中的作用，而对中枢神经系统中具有免疫功能的常驻细胞的贡献仍然知之甚少。在这项研究中，解决了胶质细胞在小鼠弓形体弓形虫感染中的作用。在病灶附近观察到活化的星形胶质细胞和小胶质细胞，并在脑实质中原位复制了寄生虫。允许弓形虫速殖子在体外感染原代小胶质细胞和星形胶质细胞。小胶质细胞允许寄生虫复制，被感染的小胶质细胞很容易跨过跨孔膜和细胞单层迁移。因此，受感染的小胶质细胞，而不是星形胶质细胞，表现出的超运动性表型让人想起最近对受感染的树突状细胞的描述。与γ干扰素激活的小胶质细胞相反，弓形虫感染的小胶质细胞不会上调主要的组织相容性复合体（MHC）II类分子和共刺激分子CD86。然而，弓形虫感染的小胶质细胞和星形胶质细胞对T细胞介导的杀伤表现出更高的敏感性，从而导致寄生虫快速地体外转移至效应T细胞。我们假设神经胶质细胞和T细胞除了在触发抗寄生虫免疫中的作用外，还可能充当“特洛伊木马”，自相矛盾地促进了弓形虫在CNS中的传播。据我们所知，这是细胞内寄生虫迁移激活驻留CNS细胞的第一个报道。

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