RIPK3 coordinates RHIM domain-dependent antiviral inflammatory transcription in neurons.

ABSTRACT: Neurons are postmitotic, nonregenerative cells that have evolved fine-tuned immunological responses to maintain life-long cellular integrity, including resistance to common programmed cell death pathways such as necroptosis. We previously demonstrated a necroptosis-independent role for the key necroptotic kinase RIPK3 in host defense against neurotropic flavivirus infection. Here, we show that RIPK3 activation had distinct outcomes in primary cortical neurons when compared with mouse embryonic fibroblasts (MEFs) during Zika virus (ZIKV) infection or after sterile activation. We found that RIPK3 activation did not induce neuronal death but instead drove antiviral gene transcription after ZIKV infection. Although RIPK3 activation in MEFs induced cell death, ablation of downstream cell death

SUBMITTER: Kofman SB 

PROVIDER: S-EPMC12042699 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature