The Hidden Diversity of Antibody Heavy Chains: Implications for Autoantibody Mediated Disease
Established Speaker: Melissa Smith, University of Louisville
Talk abstract
Current methods in Adaptive Immune Receptor Repertoire sequencing (AIRR-seq) resolve variable region sequences of antibody transcripts with minimal detailed resolution of the constant region (IGHC) therefore hindering characterization of the extent of IGHC diversity, which is known to impact downstream effector functions. Dr. Smith will present a recently developed immunogenomics tool that resolves near complete antibody heavy chain (IGH) genotypes and repertoires, near Full-Length Antibody Heavy Chain Repertoires (FLAIRR-seq). We further will present the application and potential of FLAIRR-seq, alongside it’s partner genotyping tool, IGenotyper, to identify the impact of immunogenomic variation in vaccine response, autoimmunity, and immunotherapy responses.
Speaker bio
Dr. Melissa Smith obtained her PhD in Virology at Harvard University, and continued her training in Immunology at the Institut Pastuer, Paris. She initially became interested in the potential of long-read sequencing for mapping viral evolution and immune escape in response to antibody-mediated neutralization. Dr. Smith pursued this goal, working briefly at Pacific Biosciences, developing targeted microbiology, virology, and immunology methods for single-molecule sequencing. She returned to academic research in 2016, first as Associate Director of Technology Development at the Icahn School of Medicine at Mount Sinai (New York, USA), and now as an Assistant Professor at the University of Louisville (Kentucky, USA). Today Dr. Smith focuses on utilizing innovative long-read methods for highly accurate resolution of complex genomic regions, specifically those that encode immune receptors where high levels of genomic variation can influence response to vaccination, susceptibility to autoimmunity, or development of adverse events in the context of immunotherapy.
AIRR-C Seminar Series website: [ Ссылка ]
