Keishi Fujio

CATaN integrates TF-GRNs and transcriptomes to identify genetic risk components across complex diseases, finding 588 significant CC components enriched for SNP heritability.

The paper identifies a treatment-resistant fibroblast state in RA synovitis that drives chronic inflammation through senescence-associated mechanisms and highlights therapeutic targets beyond cytokine inhibition.

Circulating miR-1285-3p in SLE promotes ABC differentiation by suppressing OXPHOS and relieving IKZF2-mediated restraint.

The paper uses population-scale Ig genetics to identify genetic associations and map their effects on the human B-cell system, revealing new genes and regulatory mechanisms in humoral immunity.

This study shows clonal overlap between Tph and Tfh cells in SLE patients and mice, suggesting shared developmental pathways and potential implications for immunosuppressive treatment.

This study identifies cell-type-specific transcriptomic signatures associated with SLE disease establishment and exacerbation, highlighting their clinical relevance and potential limitations in capturing genetic risk factors.

The paper analyzes splicing QTLs focusing on coding sequences to identify disease-causal variants associated with GWAS traits through novel integration and selection approaches.

This study conducts a trans-ancestry GWAS of rheumatoid arthritis, identifying 124 loci, 34 novel, and shows improved polygenic risk score performance across populations.