GEO series

B Cell-Intrinsic Type I Interferon Signaling Contributes to Defective Vaccine [VDJ]

GSE304899 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2026/02/19 Platform GPL24247

Summary

Affinity maturation and vaccine efficacy are compromised during chronic viral infections, yet the underlying mechanisms remain unclear. Using the LCMV Cl13 model, we show that IFN-I signaling in B cells plays a central role. IFN-I promotes early B cell activation but reduces clonal diversity and delays IgG1⁺ B cell entry into germinal centers, impairing high-affinity clone selection. Deletion of IFNAR1 in B cells partially restores NP-specific IGHV1-72 usage and GC access but fails to fully rescue affinity maturation, suggesting a contribution of extrinsic factors. Somatic hypermutation remains elevated in both genotypes, though slightly reduced in IFNAR1⁻/⁻ B cells. BASELINe analysis indicates weaker selection pressure in CDRs, potentially reflecting impaired affinity-based selection. This defect correlates with a reduced TFR/TFH ratio. Our results show that intrinsic and extrinsic IFN-I-dependent mechanisms synergize to disrupt B cell fate. These findings establish IFN-I as a key regulator of humoral immunity and highlight mechanisms underlying poor vaccine response.

Published in

B cell-intrinsic type I interferon signaling contributes to defective antibody responses to a model antigen during persistent LCMV infection

Laulhé X, Adda-Bouchard Y, Lopez G et al. · Cell reports 2026 · PMID 41865370 · doi:10.1016/j.celrep.2026.117145

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Also filed as BioProject PRJNA1295942 and SRA study SRP606664. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41865370) ↗

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