tetano
Editor, Senior Moderator
PLoS Pathog. 2016 Jul 20;12(7):e1005754. doi: 10.1371/journal.ppat.1005754. eCollection 2016.
[h=1]RIG-I Signaling Is Critical for Efficient Polyfunctional T Cell Responses during Influenza Virus Infection.[/h] Kandasamy M[SUP]1[/SUP], Suryawanshi A[SUP]2[/SUP], Tundup S[SUP]1[/SUP], Perez JT[SUP]1[/SUP], Schmolke M[SUP]3[/SUP], Manicassamy S[SUP]2[/SUP], Manicassamy B[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
PMID: 27438481 DOI: 10.1371/journal.ppat.1005754
[PubMed - in process]
[h=1]RIG-I Signaling Is Critical for Efficient Polyfunctional T Cell Responses during Influenza Virus Infection.[/h] Kandasamy M[SUP]1[/SUP], Suryawanshi A[SUP]2[/SUP], Tundup S[SUP]1[/SUP], Perez JT[SUP]1[/SUP], Schmolke M[SUP]3[/SUP], Manicassamy S[SUP]2[/SUP], Manicassamy B[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
PMID: 27438481 DOI: 10.1371/journal.ppat.1005754
[PubMed - in process]