{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T13:01:31Z","timestamp":1791205291216,"version":"4.1.0"},"reference-count":29,"publisher":"Rockefeller University Press","issue":"7","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2008,7,7]]},"abstract":"<jats:p>Immunoglobulin heavy chain (IgH) class switch recombination (CSR) replaces the initially expressed IgH C\u03bc exons with a set of downstream IgH constant region (CH) exons. Individual sets of CH exons are flanked upstream by long (1\u201310-kb) repetitive switch (S) regions, with CSR involving a deletional recombination event between the donor S\u03bc region and a downstream S region. Targeting CSR to specific S regions might be mediated by S region\u2013specific factors. To test the role of endogenous S region sequences in targeting specific CSR events, we generated mutant B cells in which the endogenous 10-kb S\u03b31 region was replaced with wild-type (WT) or synthetic 2-kb S\u03b33 sequences or a synthetic 2-kb S\u03b31 sequence. We found that both the inserted endogenous and synthetic S\u03b33 sequences functioned similarly to a size-matched synthetic S\u03b31 sequence to mediate substantial CSR to IgG1 in mutant B cells activated under conditions that stimulate IgG1 switching in WT B cells. We conclude that S\u03b33 can function similarly to S\u03b31 in mediating endogenous CSR to IgG1. The approach that we have developed will facilitate assays for IgH isotype\u2013specific functions of other endogenous S regions.<\/jats:p>","DOI":"10.1084\/jem.20080451","type":"journal-article","created":{"date-parts":[[2008,6,10]],"date-time":"2008-06-10T00:53:43Z","timestamp":1213059223000},"page":"1567-1572","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":17,"title":["S\u03b33 switch sequences function in place of endogenous S\u03b31 to mediate antibody class switching"],"prefix":"10.1084","volume":"205","author":[{"given":"Ali A.","family":"Zarrin","sequence":"first","affiliation":[{"name":"1Howard Hughes Medical Institute, Children's Hospital, Immune Disease Institute, and Department of Genetics, Harvard University Medical School, Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter H.","family":"Goff","sequence":"additional","affiliation":[{"name":"1Howard Hughes Medical Institute, Children's Hospital, Immune Disease Institute, and Department of Genetics, Harvard University Medical School, Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kate","family":"Senger","sequence":"additional","affiliation":[{"name":"2Immunology Discovery Group, Genentech Inc., South San Francisco, CA 94080"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frederick W.","family":"Alt","sequence":"additional","affiliation":[{"name":"1Howard Hughes Medical Institute, Children's Hospital, Immune Disease Institute, and Department of Genetics, Harvard University Medical School, Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2008,6,9]]},"reference":[{"key":"2023072919430012100_BIB1","doi-asserted-by":"crossref","first-page":"157","DOI":"10.1016\/S0065-2776(06)94006-1","volume":"94","year":"2007","journal-title":"Adv. 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