Jeffrey A. Sparks

This study profiles B cell activation states using multi-omics data to identify genetic mechanisms underlying immune-mediated diseases.

The paper identifies a causal allele in the CD40 locus and demonstrates context-specific trans-effects in B cells using CITE-seq and CRAFT-seq.

This study examines immune responses in adults with COVID-19 who received or did not receive nirmatrelvir-ritonavir, finding no differences in immune markers between those with and without virologic rebound.

The paper identifies activated lymphocyte phenotypes in individuals at risk for rheumatoid arthritis using mass cytometry and develops an immunophenotype score to distinguish these individuals from controls.

The paper models viral rebound after nirmatrelvir-ritonavir treatment, finding that target cell preservation and incomplete viral clearance drive rebound, with extended treatment reducing this risk.

The paper identifies functional regulatory SNPs in SLE risk loci by testing their impact on transcription factor binding and gene expression.

The paper identifies a regulatory pathway involving rs7034653, FRA2, and TRAF1 that explains how a non-coding variant increases risk of inflammatory arthritis.

The paper identifies a non-coding variant that increases ICOS expression, leading to more T peripheral helper cells and contributing to autoimmune diseases.