IL-12 bridges the early nonspecific innate immunity and the subsequent antigen-specific adaptative immunity [15] . IL-12 was shown to inhibit apoptosis of T cells [16] and of dendritic cells [17] . Alveolar macrophages have a functional IL-12 receptor, and virus-infected macrophages in the presence of IL-12 might be protected from apoptosis limiting viral clearance [18] . Apoptosis of virus-infected cells was shown to be an effective mechanism for viral clearance [19] . Bermejo-Martin and colleagues reported more significant IL-12 results in the critical A(H1N1) group of patients [9] . In our study, IL-12 is significantly higher in the nvA (H1N1)-mild disease group and in the nvA(H1N1)-ARDS group versus the control group and is not significantly higher in the bacterial ARDS group. IL-15 plays a critical role in protecting CD8 + T cells from apoptosis during the contraction phase following microbial infection [20, 21] . The CD8 + T cells surviving in the presence of IL-15 might be pathogenic in lung injury following highly pathogenic influenza A virus infection [22] . IL-15 activates the effector function of memory phenotype CD8 + cells [23] . In our study, IL-15 is significantly higher in the nvA(H1N1)-ARDS group versus the nvA(H1N1)-mild disease group, but without significant difference in the nvA(H1N1)-ARDS versus bacterial-ARDS groups. Similar to our results, IL-15 was a hallmark of critical illness in the Hong Kong and Spanish nvA(H1N1) cytokine studies [8, 9] . IL-15 is significantly higher at admission (P1) and 3 days later (P2) in the nvA(H1N1)-ARDS group for nonsurvivors versus survivors, so it might be pathogenic in lung injury influenza A virus infection. Similarly, To and colleagues found IL-15 significantly higher in critical A(H1N1) patients and very significant in the A(H1N1)-ARDS death group [8] .