Bi-directional regulation of type I interferon signaling by heme oxygenase-1.

ABSTRACT: Moderate activation of IFN-I contributes to the body's immune response, but its abnormal expression, stimulated by oxidative stress or other factors causes pathological damage. Heme oxygenase-1 (HO-1), induced by stress stimuli in the body, exerts a central role in cellular protection. Here we showed that HO-1 could promote IFN-1 under Spring Viremia of Carp virus (SVCV) infection and concomitantly attenuate the replication of SVCV. Further characterization of truncated mutants of HO-1 confirmed that intact HO-1 was essential for its antiviral function via IFN-I. Importantly, HO-1 inhibited the IFN-I signal by degrading the IRF3/7 through the autophagy pathway when it was triggered by H₂O₂ treatment. The iron ion-binding site (His28) was critical for HO-1 to degrade I

SUBMITTER: Wu M 

PROVIDER: S-EPMC10901085 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature