{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,9,26]],"date-time":"2023-09-26T06:40:17Z","timestamp":1695710417342},"reference-count":24,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,11,23]],"date-time":"2005-11-23T00:00:00Z","timestamp":1132704000000},"content-version":"vor","delay-in-days":5075,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1992,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>T lymphocytes derived from peripheral blood of a patient with adenosine deaminase (ADA) deficiency were expanded <jats:italic>in vitro<\/jats:italic>. The human ADA (hADA) gene was introduced into these replicating ADA<jats:sup>\u2212<\/jats:sup> T cells with the use of an amphotropic recombinant retrovirus carrying the hADA gene. Subsequently, infected T cells were selected on the basis of their ADA expression, by exposure to a combination of the toxic agent xylofuranosyl\u2010adenine and the specific ADA inhibitor 2\u2032\u2010deoxycoformycin. CD4<jats:sup>+<\/jats:sup> and CD8<jats:sup>+<\/jats:sup> T cells could be infected and selected with equal efficiencies. The genetically modified T cells were shown to contain intact copies of the provirus and to express normal levels of hADA. As expected, uninfected T cells from the ADA\u2010deficient patient displayed an increased sensitivity to 2\u2032\u2010deoxyadenosine. Following genetic modification, however, this sensitivity was restored to normal levels in both CD4<jats:sup>+<\/jats:sup> and CD8<jats:sup>+<\/jats:sup> T cells. The introduction of the hADA gene into the genome of the <jats:italic>in vitro<\/jats:italic> expanded T cells did not alter their phenotype, proliferative capacity or cytotoxic potential. These characteristics were identical to those of T cells derived from healthy individuals. These findings are of critical importance for the clinical application of hADA gene\u2010transducted T cells.<\/jats:p>","DOI":"10.1002\/eji.1830220111","type":"journal-article","created":{"date-parts":[[2007,3,1]],"date-time":"2007-03-01T13:01:26Z","timestamp":1172754086000},"page":"63-69","source":"Crossref","is-referenced-by-count":11,"title":["Genetic correction of cultured T cells from an adenosine deaminase\u2010deficient patient: Characteristics of non\u2010transduced and transduced T cells"],"prefix":"10.1002","volume":"22","author":[{"given":"Eric","family":"Braakman","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Victor W.","family":"Van Beusechem","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brigitte A.","family":"Van Krimpen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alain","family":"Fischer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Reinder L. 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