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Respiratory syncytial virus inhibits Type I Interferon signaling to maintain HLA-DM expression in CD1c + Dendritic cells

ABSTRACT: Respiratory Syncytial Virus (RSV) infection often elicits ineffective long-term immune responses due to inefficient immune priming, complicating disease management and vaccine development. Dendritic cells (DCs) play a pivotal role as initiators of immune responses and viral clearance. However, the direct impact of RSV on antigen presentation mechanisms remains poorly understood. In this study, we characterized the impact of RSV on blood DCs, revealing high HLA-DM expression- a unique phenotype closely associated with wider DC peptide repertoire but compromised T cell engagement during antigen presentation. We found inhibition of TBK1, a key kinase in Type I Interferon responses, restored antigen presenting capacities in RSV-infected DCs. This underscores the critical role of TBK1-mediated mechanisms in initiating adaptive immunity and downstream T cell responses during RSV infection. Our findings fill a significant knowledge gap in RSV pathogenesis, suggesting TBK1 as a potential molecular target for enhancing DC responses and immune protection against RSV.

ORGANISM(S): Homo sapiens

PROVIDER: GSE334417 | GEO | 2026/06/18

REPOSITORIES: GEO

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