{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,26]],"date-time":"2025-10-26T20:59:25Z","timestamp":1761512365783},"reference-count":36,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2005,12,8]],"date-time":"2005-12-08T00:00:00Z","timestamp":1134000000000},"content-version":"vor","delay-in-days":4908,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1992,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Mice homozygous for the <jats:italic>gld<\/jats:italic> (generalized lymphoproliferative disease) mutation develop systemic autoimmune disease and severe lymphadenopathy due to an age\u2010related accumulation in the peripheral lymphoid organs of polyclonal T cells bearing a unique phenotype (CD4<jats:sup>\u2212<\/jats:sup>CD8<jats:sup>\u2212<\/jats:sup>TCR \u03b1\u03b2<jats:sup>+<\/jats:sup>B220<jats:sup>+<\/jats:sup>). These T cells overex\u2010press T cell receptor (TcR) \u03b1\u03b2 chain RNA, proto\u2010oncogenes c\u2010myb and fyn, and proliferate poorly in response to TcR\u2010mediated stimulation. The origin of these T cells is poorly understood. To study the influence of a functionally rearranged TcR \u03b2 chain on the T cell developmental abnormality of the <jats:italic>gld<\/jats:italic> mutation and autoimmunity, we have backcrossed TcR V<jats:sub>\u03b2<\/jats:sub>8.1\u2010transgenic mice to C3H\u2010<jats:italic>gld\/gld<\/jats:italic> to homozygosity (transgenic gld mice). In transgenic gld mice, lymphadenopathy was markedly inhibited and the accumulation of CD4<jats:sup>\u2212<\/jats:sup>CD8<jats:sup>\u2212<\/jats:sup> T cells did not occur, although the remaining T cells overexpressed c\u2010myb and proliferated poorly in response to TcR occupancy. These features indicate that the pattern of proto\u2010oncogene expression and abnormal function persist in phenotypically normal T cells in transgenic gld mice, and that these characteristics can be dissociated from the accumulation of CD4<jats:sup>\u2212<\/jats:sup>CD8<jats:sup>\u2212<\/jats:sup> T cells. The hypergammaglobulinemia and anti\u2010double\u2010stranded DNA (anti\u2010dsDNA) antibody production was partially improved in transgenic gld mice, supporting the critical role of T cells in abnormal B cell activation described in autoimmunity\u2010prone mice. To investigate further the mechanisms underlying the inhibition of CD4<jats:sup>\u2212<\/jats:sup>CD8<jats:sup>\u2212<\/jats:sup> T cell accumulation in transgenic gld mice, the fetal ontogeny of T cells in transgenic mice was compared with that of non\u2010transgenic mice. In transgenic thymus, development of TcR \u03b1\u03b2<jats:sup>+<\/jats:sup> cells was accelerated as detected by earlier expression of CD4, CD8 and TcR in fetal thymus. In contrast, the number of TcR \u03b3\u03b4<jats:sup>+<\/jats:sup> cells was reduced. We suggest that altered T cell development in transgenic mice directly or indirectly inhibits the accumulation of abnormal T cells in gld mice.<\/jats:p>","DOI":"10.1002\/eji.1830220705","type":"journal-article","created":{"date-parts":[[2007,3,1]],"date-time":"2007-03-01T16:29:52Z","timestamp":1172766592000},"page":"1693-1700","source":"Crossref","is-referenced-by-count":6,"title":["Inhibition of abnormal T cell development and autoimmunity in gld mice by transgenic T cell receptor \u03b2 chain"],"prefix":"10.1002","volume":"22","author":[{"given":"Katsuyuki","family":"Yui","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Avinash","family":"Bhandoola","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shinji","family":"Komori","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Makoto","family":"Katsumata","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark I.","family":"Greene","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marko Z.","family":"Radic","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,12,8]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.159.1.1"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.1988.tb00761.x"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.iy.09.040191.001331"},{"key":"e_1_2_1_5_2","doi-asserted-by":"crossref","first-page":"4075","DOI":"10.4049\/jimmunol.136.11.4075","volume":"136","author":"Davidson W. 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