Mice that express a single transgenic T cell receptor have a low incidence of T cell lymphoma development. We investigated whether this tumor development is restricted by surveillance mechanisms that are exerted by IL-15-dependent cells. Lymphoma incidence was increased to between 30 and 60% when TCR transgenes were expressed in IL-15-deficient mice. Mice in which NK cells had been depleted genetically or with neutralizing antibodies allowed lymphoma growth while the absence of CD8 T cells was without consequence. Half of the emerged T cell lymphomas carried Notch1 mutations. The distinct phenotype of the lymphomas involved expression of PD1, CD30, CD24, the stress receptor ligand Mult1 and MHC class I down-regulation. NK cells were able to directly lyse lymphoma cells, and neutralizations of Mult1 and class I expression prevented NK cell degranulation. Together these data support an involvement of NK cells in tumor surveillance of nascent T cell lymphomas.

中文翻译：

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NK细胞可防止T细胞受体转基因小鼠中T细胞淋巴瘤的发展。

表达单个转基因T细胞受体的小鼠T细胞淋巴瘤发展的发生率较低。我们调查了这种肿瘤的发展是否受到IL-15依赖性细胞所发挥的监视机制的限制。当在IL-15缺陷型小鼠中表达TCR转基因时，淋巴瘤的发生率增加到30％至60％。NK细胞已通过基因或中和抗体耗竭的小鼠可使淋巴瘤生长，而CD8 T细胞的缺乏则没有后果。出现的T细胞淋巴瘤中有一半带有Notch1突变。淋巴瘤的独特表型涉及PD1，CD30，CD24，应激受体配体Mult1和MHC I类下调​​的表达。NK细胞能够直接裂解淋巴瘤细胞，Mult1和I类表达的中和阻止了NK细胞脱粒。这些数据共同支持了NK细胞参与新生T细胞淋巴瘤的肿瘤监测。