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

GSE334417 Homo sapiens Expression profiling by high throughput sequencing 4 samples Submitted 2026/06/18 Platform GPL34281
Summary
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.
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Direct links to NCBI, no account and no request form: the whole study as GSE334417_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 4 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1474987 and SRA study SRP706924. Searching any of these in the dataset finder brings you back here.

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