Recently, the secretion of FGL2 from naturally occurring CD4 + Foxp3 + regulatory T cells (Tregs) was demonstrated and it was reported that deficiency of Treg-produced FGL2 resulted in increased effector T cell proliferation [32] . More interestingly, Levy and colleagues showed that the frequency of FGL2 + Tregs was higher in lymphoid tissues of MHV-3 infected mice, and treatment with FGL2-specific antibodies reversed MHV-3induced liver injury and mortality in vivo. These findings demonstrated that FGL2 is an important effector cytokine of Tregs that contributes to MHV-3-induced FH [30] . PD-1 signaling has also been described as participating in regulation of Treg differentiation and function [33, 34] . In our study, we also analyzed the status of Foxp3 + cells in both PD-1-deficient and WT controls. However, the number of Foxp3-positive cells in the liver, spleen, lymph node or thymus was not significantly different between PD-1-deficient mice and their WT littermates after 72 h of MHV-3 infection (Fig. S3) . Therefore, Foxp3 + cells are unlikely to be involved in the mortality of PD-1-deficient mice. However, the functional status of these Tregs (for example, the level of FGL2 secretion) in PD-1-deficienct mice requires further investigation, and such studies are in progress in our lab.