Professor Ewha Womans Universoty Seoul, Seoul-t'ukpyolsi, Republic of Korea
Abstract Text: The Pim (proviral integration site for Moloney murine leukemia virus) proteins form a serine threonine kinase family that regulates cell proliferation, migration and cell survival. However, the role of Pim kinases in innate immune response is largely unknown. Here we demonstrate for the first time that a Pim1 kinase plays an essential role in the expression of IFN-b induced by pathogen-associated molecular patterns (PAMPs). Specifically, Pim1 is quickly upregulated after Toll-like receptor (TLR) stimulation by PAMPs in a NF-kB-dependent manner. Pim1 deficiency resulted in reduced IFN-b and IFN stimulated genes (ISGs) production. Mechanistically, Pim1 interacts with TRIF-signaling molecules and specifically regulates IFN-b induction by regulating IRF3 phosphorylation and nuclear translocation in a kinase activity-independent manner. Our study uncovers a previously unrecognized role for Pim1 in IFN-b production, thus providing a new target for controlling antiviral innate immune responses.
