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It can address key questions, including: (i) how the B\u2010cell repertoire differs in health and disease; and (ii) if it does differ, the point(s) in B\u2010cell development at which this occurs. The advent of technologies, such as whole\u2010genome sequencing, offers the chance to link abnormalities in the B\u2010cell antibody repertoire to specific genomic variants and polymorphisms. Here, we discuss the current research using B\u2010cell antibody repertoire sequencing in three polygenic autoimmune diseases where there is good evidence for a pathological role for B\u2010cells, namely systemic lupus erythematosus, multiple sclerosis and rheumatoid arthritis. These autoimmune diseases exhibit significantly skewed B\u2010cell receptor repertoires compared with healthy controls. Interestingly, some common repertoire defects are shared between diseases, such as elevated IGHV4\u201034 gene usage. B\u2010cell clones have effectively been characterized and tracked between different tissues and blood in autoimmune disease. It has been hypothesized that these differences may signify differences in B\u2010cell tolerance; however, the mechanisms and implications of these defects are not clear.<\/jats:p>","DOI":"10.1111\/imm.12927","type":"journal-article","created":{"date-parts":[[2018,3,25]],"date-time":"2018-03-25T09:53:43Z","timestamp":1521971623000},"page":"3-17","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":80,"title":["Antibody repertoire analysis in polygenic autoimmune diseases"],"prefix":"10.1111","volume":"155","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6838-0711","authenticated-orcid":false,"given":"Rachael J. 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