Moretta Lorenzo, Bottino Cristina, Pende Daniela, Vitale Massimo, Mingari Maria Cristina, Moretta Alessandro
Istituto Giannina Gaslini, Largo Gerolamo Gaslini 5, 16147 Genova-Quarto, Italy.
Trends Immunol. 2004 Dec;25(12):670-6. doi: 10.1016/j.it.2004.09.008.
After the discovery, in humans and mice, of inhibitory natural killer (NK) receptors specific for MHC class I molecules, the mechanism by which NK cells kill tumor or virus-infected cells was thought to be clarified: NK cells would kill those target cells that have lost, or underexpress, MHC class I molecules. However, a more complex scenario has recently emerged. For example, certain NK cells express insufficient amounts of triggering receptors, and target cells can lack ligands for such receptors. Thus, it appears that the activation of NK cells and their potentially harmful effector functions are under the control of different checkpoints.
在人类和小鼠中发现针对MHC I类分子的抑制性自然杀伤（NK）受体后，NK细胞杀伤肿瘤或病毒感染细胞的机制被认为已得到阐明：NK细胞会杀伤那些已经丢失或低表达MHC I类分子的靶细胞。然而，最近出现了一种更为复杂的情况。例如，某些NK细胞表达的触发受体数量不足，而靶细胞可能缺乏此类受体的配体。因此，似乎NK细胞的激活及其潜在的有害效应功能受到不同检查点的控制。
