自然杀伤（NK）细胞与移植物抗宿主病（GVHD）：在小鼠P----F1模型中，NK细胞水平与GVHD之间无相关性。
Natural killer (NK) cells and graft-versus-host disease (GVHD): no correlation between the NK cell levels and GVHD in the murine P----F1 model.
作者信息
Varkila K, Hurme M
出版信息
Immunology. 1985 Jan;54(1):121-6.
Graft-versus-host disease (GVHD) was induced in (CBA X C57BL/6) F1 mice by i.v. injection of 50 X 10(6) parental spleen cells. The GVHD induced an enhanced NK (anti-YAC-1) cytotoxicity during the first 2 weeks after the spleen cell transfusion. This cytotoxic activity was shown to be mediated by asialo GM1-positive, partially Thy-1-positive and nylon-wool (NW) non-adherent cells, thus being classical NK cells. Depletion of NK-cell activity from donor and/or recipient mice with anti-asialo GM1 antibody prior to the spleen cell transfer did not prevent the GVHD as judged by the splenomegaly assay. Also, when NK activity was potentiated with polyinosinic-polycytidylic acid (pIC), no effect on the GVHD was seen. These data suggest that NK cells are not crucial for the development of GVHD in this model.
通过静脉注射50×10⁶个亲代脾细胞，在（CBA×C57BL/6）F1小鼠中诱导移植物抗宿主病（GVHD）。在脾细胞输注后的前2周内，GVHD诱导了增强的NK（抗YAC-1）细胞毒性。这种细胞毒性活性被证明是由去唾液酸GM1阳性、部分Thy-1阳性和尼龙毛（NW）非黏附细胞介导的，因此是经典的NK细胞。在脾细胞转移前，用抗去唾液酸GM1抗体耗尽供体和/或受体小鼠的NK细胞活性，通过脾肿大测定判断并不能预防GVHD。此外，当用聚肌苷酸-聚胞苷酸（pIC）增强NK活性时，未观察到对GVHD有影响。这些数据表明，在该模型中，NK细胞对于GVHD的发展并非至关重要。
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