Suzuki Yasuhiro
Center for Molecular Medicine/Infectious Diseases, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, 1410 Prices Fork Road, Blacksburg, VA 24061, USA.
J Infect Dis. 2002 Dec 1;186 Suppl 2:S234-40. doi: 10.1086/344276.
Interferon (IFN)-gamma is an absolute requirement for resistance against acute acquired infection with Toxoplasma gondii and development of toxoplasmic encephalitis (TE) during the late stage of infection. Multiple populations of both T and non-T cells are important sources of IFN-gamma in resistance. In the absence of IFN-gamma-producing non-T cells, T cells cannot prevent TE. Interleukin-12, Bcl-3, NF-kappaB(2), and CD40-CD40L ligand interaction are important for up-regulation of IFN-gamma production. T. gondii infects a variety of host cells, and IFN-gamma-mediated immune responses control the parasite in both phagocytic and nonphagocytic cells through at least five different mechanisms, most likely depending on the types of cells responding to IFN-gamma. Such effector functions involve production of NO by iNOS, tryptophan degradation by the enzyme IDO (indolamine 2,3-dioxygenase), unidentified mechanism(s) mediated by 47- to 48-kDa proteins encoded by an IFN-gamma responsive gene family, limiting the availability of intracellular iron to the parasite, and production of reactive oxygen intermediates.
γ干扰素（IFN-γ）是抵抗刚地弓形虫急性获得性感染以及感染后期弓形虫性脑炎（TE）发展的绝对必要条件。多种T细胞群和非T细胞群是抵抗过程中IFN-γ的重要来源。在缺乏产生IFN-γ的非T细胞时，T细胞无法预防TE。白细胞介素-12、Bcl-3、NF-κB(2)以及CD40-CD40L配体相互作用对于上调IFN-γ的产生很重要。刚地弓形虫感染多种宿主细胞，IFN-γ介导的免疫反应通过至少五种不同机制在吞噬细胞和非吞噬细胞中控制该寄生虫，很可能取决于对IFN-γ作出反应的细胞类型。此类效应功能包括诱导型一氧化氮合酶（iNOS）产生一氧化氮、吲哚胺2,3-双加氧酶（IDO）对色氨酸的降解、由IFN-γ反应基因家族编码的47至48 kDa蛋白质介导的未知机制、限制寄生虫的细胞内铁供应以及产生活性氧中间体。
