Previous studies have shown that the secretion of FGL2 can be triggered by the pro-inflammatory factors IFN-c and TNF-a [21, 22] . On the other hand, the production of IFN-c and TNF-a by activated T cells, NK cells and macrophages can be inhibited by the PD-1 signal [6] . Therefore, we compared the status of IFNc and TNF-a in PD-1-deficient and WT mice in response to MHV-3 infection. qPCR revealed that the transcription of the IFN-c gene in liver was significantly higher in PD-1-deficient mice than in WT mice at 72 h post-MHV-3 infection (Fig. 6B) . In PD-1-deficient spleen, the transcription of both IFN-c and TNF-a was found to be rapidly enhanced upon MHV-3 exposure (Fig. 6C ). FACs analysis indicated that IFN-c secretion from NK cells, but not from CD3 + T cells, in the liver was much higher in PD-1deficient mice at 72 h after MHV-3 infection (Fig. 6D ). The fact that IFN-c and TNF-a both have the capacity to initiate FGL2 expression may explain why higher FGL2 expression was observed in the PD-1-deficient mice.