Ludvig Magne Sollid

The paper shows that IEC-derived TG2-DGP fusion protein drives anti-TG2 autoantibody production in celiac disease.

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.

This study identifies 13 novel genetic associations for celiac disease, with the 5p15.33 locus showing strong potential, and links IRX1 to rheumatoid arthritis.

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.

immuneML provides an open-source ecosystem for reproducible and interoperable machine learning analysis of adaptive immune receptor repertoires, demonstrating its utility through benchmarking and novel methods.

The paper identifies 48 novel light chain variable gene polymorphisms in a Norwegian cohort and finds partial intron retention in alternative splice variants of low-expressed genes.

The paper identifies TRAFD1 as a master regulator of IFNγ signalling in celiac disease by systematically prioritizing candidate genes in disease loci using multiple computational methods.

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.