Ida Lindeman

The paper examines systemic and gut IgA responses to bacteria in the human upper gastrointestinal tract, finding distinct reactivity patterns and limited clonal overlap between gut and bone marrow plasma cells.

The paper shows HLA-DQ2.5 variants increase frequencies of TCR genes involved in gluten epitope recognition in CeD patients, linking HLA to disease by shaping the naive TCR repertoire.

The paper identifies circulating TG2-specific IgA cells in celiac disease patients, showing they are clonally related to intestinal plasma cells and generated via an extrafollicular response involving gluten-specific CD4+ T cells.

The paper develops a Bayesian haplotyping method to infer V-D-J haplotypes and deletion patterns in the human antibody heavy chain gene locus using antibody repertoire sequencing data.

BraCeR reconstructs B-cell receptor sequences and infers clonality from scRNA-seq data without needing additional Rep-seq.