Aliberti Julio
Department of Immunology, Duke University Medical Center, Durham, North Carolina 27705, USA.
Nat Rev Immunol. 2005 Feb;5(2):162-70. doi: 10.1038/nri1547.
Hosts that are infected with Toxoplasma gondii must mount a powerful immune response to contain dissemination of the parasite and to prevent mortality. After parasite proliferation has been contained by interferon-gamma-dependent responses, the onset of the chronic phase of infection is characterized by continuous cell-mediated immunity. Such potent responses are kept under tight control by a class of anti-inflammatory eicosanoid, the lipoxins. Here, we review such immune-containment strategies from the perspective of the host, which attempts to keep pro-inflammatory responses under control during chronic disease, as well as from the perspective of the pathogen, which hijacks the lipoxygenase machinery of the host for its own advantage, probably as an immune-escape mechanism.
感染刚地弓形虫的宿主必须启动强大的免疫反应,以抑制寄生虫的传播并防止死亡。在寄生虫增殖被干扰素-γ依赖的反应抑制后,感染慢性期的开始以持续的细胞介导免疫为特征。这类有效的反应受到一类抗炎类二十烷酸——脂氧素的严格控制。在这里,我们从宿主的角度综述这种免疫抑制策略,宿主试图在慢性疾病期间控制促炎反应,同时也从病原体的角度进行综述,病原体利用宿主的脂氧合酶机制为自身谋利,这可能是一种免疫逃逸机制。