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All the patient's IgM heavy\u2010chain and \u03ba light\u2010chain transcripts were functional, suggesting that either non\u2010functional rearrangements were being selectively class\u2010switched to IgG, or that receptor editing was rendering genes non\u2010functional after class\u2010switching. The functional \u03b3\u2010chain sequences showed a normal rate of somatic hypermutation while non\u2010functional sequences contained few somatic mutations, suggesting that most came from cells that had no functional gene and therefore were not receiving signals for hypermutation. However, apoptosis of peripheral blood lymphocytes was not impaired. No defects have been found in any of the genes currently known to be responsible for hyper\u2010IgM syndrome but the phenotype fits best to type 4.<\/jats:p>","DOI":"10.1111\/j.0019-2805.2003.01790.x","type":"journal-article","created":{"date-parts":[[2004,1,21]],"date-time":"2004-01-21T16:15:46Z","timestamp":1074701746000},"page":"212-222","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Non\u2010functional immunoglobulin G transcripts in a case of hyper\u2010immunoglobulin M syndrome similar to type 4"],"prefix":"10.1111","volume":"111","author":[{"given":"John M.","family":"Darlow","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alex M.","family":"Farrell","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David I.","family":"Stott","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2004,1,21]]},"reference":[{"key":"e_1_2_7_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-5699(97)01086-4"},{"issue":"1","key":"e_1_2_7_3_2","first-page":"1","article-title":"Primary immunodeficiency diseases. 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