Pathways:
RIG-I/MAVS/IFNAR1 pathway
Host Molecules Involved:
Eight “suppressor of cytokine signaling” (SOCS) regulatory proteins
Influenza Strain:
Influenza A virus (IAV)
Tissues:
Human respiratory epithelial cells
Interactions:
SOCS1 and SOCS3, RIG-I/MAVS/IFNAR1 pathway
Mechanisms:
- SOCS1 to SOCS7 are constitutively expressed in IAV-infected cells.
- SOCS1 and SOCS3 expressions are up-regulated after IAV infection.
- SOCS1 and SOCS3 up-regulation needs a TLR3-independent, retinoic acid-inducible gene I (RIG-I)/mitochondrial antiviral signaling protein (MAVS)/IFNalphabeta receptor (IFNAR)1-dependent pathway.
- SOCS1 and SOCS3 inhibit antiviral responses, and differentially regulate inflammatory signaling pathways.
- MAVS is a RIG-I signaling intermediate.
Effects:
Innate immune response to influenza A virus infection is inhibited by SOCS1 and SOCS3 via the RIG-I/MAVS/IFNAR1-dependent pathway.
Reference:
Pothlichet, J., Chignard, M., et al. (2008) Cutting edge: innate immune response triggered by influenza A virus is negatively regulated by SOCS1 and SOCS3 through a RIG-I/IFNAR1-dependent pathway. J Immunol 180, 2034-2038.
