Linda S. Wicker

The paper identifies CD8+FOXP3+ Tregs enriched in human tissues, expressing intracellular CD25 and tissue residency markers, and demonstrates their therapeutic potential and association with disease states.

The paper investigates how HLA-DQβ157 polymorphism influences T cell receptor selection and links it to microbial antigens that mimic insulin, contributing to type 1 diabetes pathogenesis.

The paper shows that HLA class II haplotypes influence T1D risk by selecting for CD4+ T cell receptors with negatively charged CDR3β sequences that bind insulin, and demonstrates this in peripheral and islet T cells.

This study identifies causal variants, cells, genes, and drug targets for type 1 diabetes using large-scale genetic and functional genomic analyses.

The paper uses single-cell multi-omics to analyze T and NK cells in SLE patients, identifying IFN-driven changes and novel biomarkers.

The paper identifies genetic risk factors associated with early-onset type 1 diabetes, showing stronger effects in children diagnosed before age 7 compared to those diagnosed at 13 or older.

This paper introduces a Bayesian joint fine-mapping method that improves accuracy in identifying causal variants across related immune-mediated diseases by leveraging shared genetic information.

The paper identifies autoimmune disease candidate genes by integrating promoter capture Hi-C data with genetic associations in activated CD4+ T cells.

The paper identifies SNP rs61839660 as the causal variant for autoimmunity by showing its loss reduces IL2RA expression and T1D protection.