RIG-I Signaling Is Critical for Efficient Polyfunctional T Cell Responses during Influenza Virus Infection

Retinoic acid inducible gene-i (rig-i) is an innate rna sensor that recognizes the influenza a virus (iav) rna genome and activates antiviral host responses. here,we demonstrate that rig-i signaling plays a crucial role in restricting iav tropism and regulating host immune responses. mice deficient in the rig-i-mavs pathway show defects in migratory dendritic cell (dc) activation,viral antigen presentation,and priming of cd8+ and cd4+ t cell responses during iav infection. these defects result in decreased frequency of polyfunctional effector t cells and lowered protection against heterologous iav challenge. in addition,our data show that rig-i activation is essential for protecting epithelial cells and hematopoietic cells from iav infection. these diverse effects of rig-i signaling are likely imparted by the actions of type i interferon (ifn),as addition of exogenous type i ifn is sufficient to overcome the defects in antigen presentation by rig-i deficient bmdc. moreover,the in vivo t cell defects in rig-i deficient mice can be overcome by the activation of mda5 –mavs via poly i:c treatment. taken together,these findings demonstrate that rig-i signaling through mavs is critical for determining the quality of polyfunctional t cell responses against iav and for providing protection against subsequent infection from heterologous or novel pandemic iav strains. © 2016 kandasamy et al.