Kamiyama T, Tatsumi M
Infect Immun. 1983 Nov;42(2):789-95. doi: 10.1128/iai.42.2.789-795.1983.
Thymocytes from mice 2 weeks after infection with Toxoplasma gondii resisted natural killer (NK) cell-mediated cytolysis in contrast to the high sensitivity of normal mouse thymocytes. The infected mouse thymocytes also failed to form conjugates with effector cells and to compete for cytolysis of NK sensitive targets. These effects were mediated, at least in part, by interferon-gamma because normal thymocytes became NK insensitive after incubation in the infected mouse serum which contained significant amount of interferon-gamma, and pH 2 treatment of the serum abolished the effect. An alternate possibility for the reduced NK sensitivity of the infected mouse thymocytes was the elimination of NK-sensitive cells from the thymus, since histopathological studies showed marked atrophy and clearance of NK-sensitive thymocytes in the cortex of thymuses of infected mice. Although T. gondii induced augmentation followed by suppression of the host splenic NK activity, it seems unlikely that this altered NK activity was responsible for the lowered NK sensitivity of the thymocytes.
与正常小鼠胸腺细胞的高敏感性相比，感染刚地弓形虫2周后的小鼠胸腺细胞对自然杀伤（NK）细胞介导的细胞溶解具有抗性。受感染的小鼠胸腺细胞也无法与效应细胞形成结合物，并且无法竞争对NK敏感靶标的细胞溶解。这些效应至少部分是由γ干扰素介导的，因为正常胸腺细胞在含有大量γ干扰素的受感染小鼠血清中孵育后对NK变得不敏感，并且血清经pH 2处理后消除了这种效应。受感染小鼠胸腺细胞NK敏感性降低的另一种可能性是胸腺中NK敏感细胞的消除，因为组织病理学研究显示受感染小鼠胸腺皮质中NK敏感胸腺细胞明显萎缩和清除。尽管刚地弓形虫诱导宿主脾脏NK活性先增强后抑制，但这种改变的NK活性似乎不太可能是胸腺细胞NK敏感性降低的原因。
