{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lobb TA"],"funding":["NIDA NIH HHS","NIAID NIH HHS","NHLBI NIH HHS","ORFDO NIH HHS"],"pagination":["41"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12873219"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(1)"],"pubmed_abstract":["Type I interferons (IFN) are key mediators of innate immune activation, promoting upregulation of costimulatory molecules and Major Histocompatibility Complex (MHC) I/II on antigen-presenting cells (APCs). However, IFN also suppress endogenous translation to restrict viral replication. Critically, IFN-stimulated APCs lose the capacity to acquire new antigens, making the timing of IFN signaling a crucial determinant of vaccine efficacy. Here, we show that both DC-specific loss of IFNα/β receptor (IFNαR) and transient blockade of IFNαR before vaccination enhances vaccine uptake and expression within DCs, improves CD8⁺ T cell priming, and leads to superior tumor control. We also demonstrate that IFN signaling before vaccination, triggered by prior infection or administration of a different va"],"journal":["NPJ vaccines"],"pubmed_title":["Type I interferon restricts mRNA vaccine efficacy through suppression of antigen uptake in cDCs."],"pmcid":["PMC12873219"],"funding_grant_id":["75N99020D00005","75N95020D00005","75N93022D00005","75N92020D00005","75N93023D00005"],"pubmed_authors":["DiPaolo RJ","Ferris ST","Dickson A","Carrero JA","Guo W","Dalben Y","Alspach E","Tse LV","Lobb TA","Beeram S"],"additional_accession":[]},"is_claimable":false,"name":"Type I interferon restricts mRNA vaccine efficacy through suppression of antigen uptake in cDCs.","description":"Type I interferons (IFN) are key mediators of innate immune activation, promoting upregulation of costimulatory molecules and Major Histocompatibility Complex (MHC) I/II on antigen-presenting cells (APCs). However, IFN also suppress endogenous translation to restrict viral replication. Critically, IFN-stimulated APCs lose the capacity to acquire new antigens, making the timing of IFN signaling a crucial determinant of vaccine efficacy. Here, we show that both DC-specific loss of IFNα/β receptor (IFNαR) and transient blockade of IFNαR before vaccination enhances vaccine uptake and expression within DCs, improves CD8⁺ T cell priming, and leads to superior tumor control. We also demonstrate that IFN signaling before vaccination, triggered by prior infection or administration of a different va","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-07-15T13:33:27.77Z","creation":"2026-07-05T03:08:22.022Z"},"accession":"S-EPMC12873219","cross_references":{"pubmed":["41486285"],"doi":["10.1038/s41541-025-01362-z"]}}