Department of Immunoparasitology, Research Institute for Microbial Diseases, Osaka University, Yamadaoka, Suita, Osaka, Japan.
Laboratory of Immunoparasitology, WPI Immunology Frontier Research Center, Osaka University, Yamadaoka, Suita, Osaka, Japan.
Int Immunol. 2018 Mar 10;30(3):113-119. doi: 10.1093/intimm/dxy004.
Toxoplasma gondii can infect homoeothermic animals including humans and cause lethal toxoplasmosis in immunocompromised individuals. When hosts are infected with T. gondii, the cells induce immune responses against T. gondii. The pathogen infection is recognized by immune sensors that directly detect T. gondii structural components, leading to production of pro-inflammatory cytokines and chemokines. Antigen-presenting cells such as macrophages and dendritic cells strongly activate T cells and induce development of Th1 cells and antigen-specific killer CD8 T cells. These T cells and Group 1 innate lymphoid cells are main producers of IFN-γ, which robustly stimulates cell-autonomous immunity in cells infected with T. gondii. IFN-γ-inducible effectors such as IFN-inducible GTPases, inducible nitric oxide synthase and indoleamine-2,3-dioxygenase differentially play important roles in suppression of T. gondii growth and its direct killing in anti-T. gondii cell-autonomous immune responses. In this review, we will describe our current knowledge of innate, adaptive and IFN-γ-mediated cell-autonomous immunity against T. gondii infection.
刚地弓形虫可感染恒温动物,包括人类,并在免疫功能低下的个体中引起致命的弓形体病。当宿主感染刚地弓形虫时,细胞会针对刚地弓形虫产生免疫反应。病原体感染被免疫传感器识别,这些传感器可直接检测刚地弓形虫的结构成分,导致促炎细胞因子和趋化因子的产生。抗原呈递细胞(如巨噬细胞和树突状细胞)可强烈激活 T 细胞,并诱导 Th1 细胞和抗原特异性杀伤性 CD8 T 细胞的发育。这些 T 细胞和 ILC1 是 IFN-γ的主要产生者,可强烈刺激刚地弓形虫感染细胞中的细胞自主免疫。IFN-γ诱导的效应物,如 IFN 诱导的 GTP 酶、诱导型一氧化氮合酶和吲哚胺 2,3-双加氧酶,在抑制刚地弓形虫生长及其在抗刚地弓形虫细胞自主免疫反应中的直接杀伤方面发挥着重要作用。在这篇综述中,我们将描述我们目前对针对刚地弓形虫感染的先天、适应性和 IFN-γ介导的细胞自主免疫的认识。