Journal
IMMUNOLOGY
Volume 169, Issue 3, Pages 369-383Publisher
WILEY
DOI: 10.1111/imm.13637
Keywords
influenza B virus; interferon beta; Pellino3 ligase; RIG-I; TRAF3
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Viral infection triggers the innate immune system to produce pro-inflammatory cytokines through pattern recognition receptors. The role of Pellino3 in antibacterial and antiviral response is important but not well understood. This study investigates the involvement of Pellino3 in the RIG-I-dependent signaling pathway during influenza B virus infection. The results suggest that Pellino3 mediates the ubiquitination and degradation of TRAF3, thereby suppressing IRF3 activation and IFNβ production.
Viral infection activates the innate immune system, which recognizes viral components by a variety of pattern recognition receptors and initiates signalling cascades leading to the production of pro-inflammatory cytokines. To date, signalling cascades triggered after virus recognition are not fully characterized and are investigated by many research groups. The critical role of the E3 ubiquitin ligase Pellino3 in antibacterial and antiviral response is now widely accepted, but the precise mechanism remains elusive. In this study, we sought to explore Pellino3 role in the retinoic acid-inducible gene I (RIG-I)-dependent signalling pathway. In this work, the molecular mechanisms of the innate immune response, regulated by Pellino3, were investigated in lung epithelial cells during influenza B virus infection. We used wild-type and Pellino3-deficient A549 cells as model cell lines to examine the role of Pellino3 ligase in the type I interferon (IFN) signalling pathway. Our results indicate that Pellino3 is involved in direct ubiquitination and degradation of the TRAF3, suppressing interferon regulatory factor 3 (IRF3) activation and interferon beta (IFN beta) production.
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