L. M. Sollid

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 AIRRTM, a generative model that identifies and generates disease-associated adaptive immune receptor sequences using only repertoire-level immune status data.

The paper identifies separate gut plasma cell populations in DH patients producing autoantibodies specific to TG2 and TG3 with no cross-reactivity.

The paper identifies a new native gluten epitope recognized by cross-reactive B cells in celiac disease, which may contribute to epitope spreading.

The paper identifies KIR+CD8+ T cells as regulatory cells in humans that suppress pathogenic CD4+ T cells in autoimmune and infectious diseases.

The paper describes the engineering of high-affinity human antibodies that recognize gluten epitopes bound to HLA-DQ2.5 and inhibit T-cell activation in celiac disease.

This study links IgG constant region polymorphisms to stereotyped B-cell responses in multiple sclerosis by analyzing clonal relationships and isotype distributions in intrathecal B-lineage cells.

The paper shows that VDJ recombination rules vary between individuals, leading to individual-specific Ig sequence spaces.

The paper uses machine learning to analyze naive B-cell receptor repertoires to distinguish celiac disease patients from controls, achieving an F1 score of 85%.

The paper analyzes single-cell RNA-seq data from plasma cells in celiac disease patients to identify transcriptional differences and clonal relationships between disease-specific and non-specific plasma cells.

The paper identifies novel germline IGHV alleles and upstream sequence variability, challenging current immunoglobulin repertoire annotation methods.

The paper identifies that most CD8 T cells in the human small intestine are resident memory cells that persist for over a year and maintain a stable TCR repertoire.