The main site of infection for influenza viruses is the respiratory epithelium. The first line of defense is performed by the innate immune system which is rapid but lacks specificity and memory. Innate immunity is formed by physical barriers (e.g., mucus and collectins) and innate cellular immune responses. The virus infects the epithelial cells then spreads to leukocytes such as macrophages, dendritic cells (DCs), and Natural Killer (NK) cells. Infected cells recognize viral PAMPS (pathogen associated molecular patterns) through cell specific PPRs (pattern recognition receptors).There are three families of receptors that recognize viral PAMPs: TLRs (toll-like receptors), RIG-I (retinoic acid inducible gene I), and NOD-like (nucleotide oligomerization domain-like) receptors. Although host responses to infection are critical for final viral clearance and stimulation of adaptive immune responses, an exacerbated response can lead to immunopathology and severe disease. For example, high levels of neutrophil extracellular traps (chromatin-based structures released from neutrophils) can lead to lung damage and severe influenza virus infection. Therapies aimed to reduce these exacerbations which are called cytokine storm might be beneficial for patients with severe influenza. Here we would like to give an overview about Immune response to Influenza virus.