ArticleNPJ vaccines2026
Type I interferon restricts mRNA vaccine efficacy through suppression of antigen uptake in cDCs.
Article in NPJ vaccines, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Unlocking translational resilience for mRNA vaccines by viral UTRs.Molecular therapy. Nucleic acids · 2026Article
- mRNA vaccines engage unconventional pathways in CD8Nature · 2026Article
- Engineering a safe and potent LNP-mRNA delivery system by leveraging the dual activities of α-tocopherol.International journal of pharmaceutics: X · 2026Article
- Inhibition of Exo70, an Exocyst Complex Component, Enhances mRNA Delivery Efficiency of Lipid Nanoparticle.Pharmaceutics · 2026Article
- Dissecting the mechanism of action of the adjuvant system AS01 in human immune cells: synergy of QS-21 and monophosphoryl lipid A and role of type I interferons.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
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 vaccine, impairs dendritic cell uptake of mRNA-LNP vaccines and reduces the magnitude of vaccine-specific CD8⁺ T cell responses. These findings highlight the dual-edged nature of IFN signaling and offer a potential strategy for enhancing vaccine-induced immunity.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.