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In this study, we found that\n            <jats:italic>\n              runx1\n              <jats:sup>W84X\/W84X<\/jats:sup>\n            <\/jats:italic>\n            mutation led to the reduction and disordering of B cells, as well as the failure of V(D)J rearrangements in B cells but not T cells, resulting in antibody-inadequate-mediated immunodeficiency in adult zebrafish. By contrast, T cell development was not affected. The decreased number of B cells mainly results from excessive apoptosis in immature B cells. Disrupted B cell development results in\n            <jats:italic>\n              runx1\n              <jats:sup>W84X\/W84X<\/jats:sup>\n            <\/jats:italic>\n            mutants displaying a similar phenotype to common variable immunodeficiency\u2014a primary immunodeficiency disease primarily characterized by frequent susceptibility to infection and deficient immune response, with marked reduction of antibody production of IgG, IgA and\/or IgM. Our studies demonstrated an evolutionarily conserved function of\n            <jats:italic>runx1<\/jats:italic>\n            in maturation and differentiation of B cells in adult zebrafish, which will serve as a valuable model for the study of immune deficiency diseases and their treatments.\n          <\/jats:p>","DOI":"10.1098\/rsob.180043","type":"journal-article","created":{"date-parts":[[2018,7,25]],"date-time":"2018-07-25T07:25:24Z","timestamp":1532503524000},"update-policy":"https:\/\/doi.org\/10.1098\/crossmark-policy","source":"Crossref","is-referenced-by-count":14,"title":["Loss of\n            <i>runx1<\/i>\n            function results in B cell immunodeficiency but not T cell in adult zebrafish"],"prefix":"10.1098","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9325-3271","authenticated-orcid":false,"given":"Yali","family":"Chi","sequence":"first","affiliation":[{"name":"Key Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases of 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