the immune response , Th0 cells differentiate to Th2  cells, which secrete IL-4, IL-5, IL-6 and help preferentially drive IgG1, IgA and IgE Ab production by anti- body-secreting plasma cells (ASCs) [6] [7] [8] [9] . CD8+ precursor T-cells, which maturate into CTLs (cytotoxic T lymphocytes), release antiviral cytokines (IFN-γ) upon recognition of short viral peptides presented by MHC I molecules on virus-infected epithelial cells, and destroy the virus infected cells by exocytosis of cytolytic granules. The granules contain cytolytic protein perforin and granzymes. Perforin is a protein that creates pores in membranes of infected cells. Granzymes are members of serine protease family. In the presence of perforin, granzymes enter into the cytoplasm of infected cells and initiate proteolysis, which triggers destruction of the target cell [10, 11] . CTLs could mediate killing of infected cells also by perforin-independent mechanisms of cytotoxicity. This involves binding of Fas receptor in the infected target cell membranes with the Fas ligand (FasL) expressed on activated CTLs. Interaction of FasL with corresponding Fas receptor leads to the activation of caspases, which induce apoptosis in influenza infected cells [12] [13] [14] .