Immunoglobulin (IG) and T-cell receptor (TR) loci are formed by expanded families of variable (V), diversity (D), and joining (J) genes that encode adaptive immune agents through a complex of somatic processes collectively called V(D)J recombination. Adaptive immune loci are subject to rapid evolution that results in an extremely high diversity of germline V, D, and J genes. This diversity complicates the detection of germline V, D, J genes and makes the development of robust gene nomenclatures challenging. Our goals is to develop tools for annotating highly diverse IG/TR loci and transparent naming IG/TR genes.
A high diversity of adaptive immune loci complicates comparative analysis of adaptive immune responses across vertebrate species aiming at answering questions like "what makes one species susceptible to a disease, while its close relative is immune to it?" or "what makes some species reservoirs for pathogens?". To answer these questions, we are developing approaches and tools enabling comparative and evolutionary analyses of adaptive immune systems that utilize sequencing data from germline IG/TR loci and expressed adaptive immune repertoires as well as functional data such as antibody titers and scRNA-seq.
Recent studies showen that individual polymorhisms in germline IG/TR loci shape adaptive immune responses and can be associated with responses to vaccines and disease susceptibility. These observations are deeply connected to the personalized approach in medicine as they are related to questions "How to identify individuals who do not respond to a vaccine?" and "How to reveal individuals vulnerable to a disease?". Answering these questions would enable designing vaccines targeting non-responsive subjects and finding immunogenomics markers for early revealing the disease susceptibility.