Influenza infection induces specific humoral immunity represented by systemic and local antibody response, as well as cellular immunity, represented by specific T-cell response ( Figure 1 ). Both of them are important in the host defense against influenza infection, because of their close cooperation mediated by various immune mechanisms. Dendritic cells and macrophages (antigen presenting cells, APCs) play an important role in initiating and driving of adaptive immune response [4] . Exogenous viral antigens, including inactive viral particles, intact viruses or infected cells, are taken up by APCs through endocytosis or phagocytosis. Their further processing results in generation of peptides that are presented via MHC I or MHC II molecules to CD8+ precursor T-cell and CD4+ helper T-cell precursors (Th0), respectively. Th0 cells are subdivided to Th1and Th2-type helper cells, based on the cytokine profiles they produce. Following influenza infection, APCs secrete IL-12 that contributes to the differentiation of Th0 into Th1 cells, which secrete IFN-γ and help to produce IgG2a antibodies [5, 6] . Th1 cells also produce IL-2, required for the proliferation of the virus-specific CD8+ CTLs. In contrast, when IL-10 is present early in The cellular immune response (right) is initiated after recognition of viral antigens presented via MHCI and MHC II molecules by antigen presenting cells (APC), which then leads to activation, proliferation and differentiation of antigen-specific CD8+ T or CD4+ cells. These cells gain effector cell function and either they help directly (Th1 or Th2 cell) to produce antibodies or, CTL effector cells recognize antigen peptides presented by MHCI on APC and kill the virus infected cells by exocytosis of cytolytic granules. The humoral immune response (left)is mediated by specific antibodies (e.g IgG, IgA) produced by antibody secreting plasma cells (ASC) which are the final stage of B cell development. This process is aided by CD4+ T helper and T cell-derived cytokines essential for the activation and differentiation of both B-cell responses and CD8+ T cell responses.