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

Kandasamy, Matheswaran
Suryawanshi, Amol
Tundup, Smanla
Perez, Jasmine T
Manicassamy, Santhakumar
Manicassamy, Balaji
Published in PLOS Pathogens. 2016, vol. 12, no. 7, p. e1005754
Abstract 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
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Article (Published version) (3.3 MB) - public document Free access
Research group Intéractions entre les pathogènes viraux et bactériens (947)
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KANDASAMY, Matheswaran et al. RIG-I Signaling Is Critical for Efficient Polyfunctional T Cell Responses during Influenza Virus Infection. In: PLOS Pathogens, 2016, vol. 12, n° 7, p. e1005754. https://archive-ouverte.unige.ch/unige:89729

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Deposited on : 2016-12-02

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