{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T15:47:51Z","timestamp":1770738471796,"version":"3.49.0"},"reference-count":0,"publisher":"Rockefeller University Press","issue":"3","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1988,3,1]]},"abstract":"<jats:p>The lpr gene induces marked lymphoproliferation characterized by the massive accumulation of T cells of an unusual phenotype and concomitant autoimmune disease. To clarify the mechanism of the lpr effect, bone marrow cells from B6-lpr\/lpr (Ly-1.2) and B6-+\/+ (Ly-1.1) mice were transferred into lethally irradiated B6-lpr\/lpr mice. As has been previously reported, recipients of the B6-lpr\/lpr bone marrow showed the typical lpr phenotype with marked lymphadenopathy, splenomegaly and increased levels of autoantibodies; while the recipients of B6-+\/+ bone marrow had normal sized lymph nodes and spleen and no autoantibodies. A third group of mice received an equal mixture of bone marrow cells from the B6-lpr\/lpr and B6-+\/+ donors. These mice showed both lymphadenopathy and autoantibody production comparable to that of recipients of the B6-lpr\/lpr marrow alone. Immunofluorocytometric analysis of the lymphoid populations in these mixed bone marrow recipients established that the T cells from the lpr\/lpr and +\/+ donors were equivalently represented in the peripheral blood and thymus. In striking contrast, the T cells that accumulated in abnormally large numbers in the lymph nodes were almost entirely from the lpr donor. Their surface phenotype was Thy-1+(dull), Ly-1.2+(dull), Lyt-2-, L3T4-, 9F3+, and 3A1+, which is consistent with that found in intact lpr mice. These results indicate that the lpr gene causes an intrinsic defect directly within the T cells that accumulate in large numbers in lpr mice. In addition, the presence of the +\/+ T cells cannot prevent the expression of the lpr abnormalities.<\/jats:p>","DOI":"10.1084\/jem.167.3.741","type":"journal-article","created":{"date-parts":[[2004,6,24]],"date-time":"2004-06-24T07:56:10Z","timestamp":1088063770000},"page":"741-751","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":30,"title":["The lpr gene causes an intrinsic T cell abnormality that is required for hyperproliferation."],"prefix":"10.1084","volume":"167","author":[{"given":"T","family":"Katagiri","sequence":"first","affiliation":[{"name":"Department of Medicine, University of North Carolina, Chapel Hill 27599."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P L","family":"Cohen","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of North Carolina, Chapel Hill 27599."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R A","family":"Eisenberg","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of North Carolina, Chapel Hill 27599."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"291","published-online":{"date-parts":[[1988,3,1]]},"container-title":["The Journal of experimental medicine"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/rupress.org\/jem\/article-pdf\/167\/3\/741\/1668436\/741.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/rupress.org\/jem\/article-pdf\/167\/3\/741\/1668436\/741.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,7,25]],"date-time":"2023-07-25T01:17:29Z","timestamp":1690247849000},"score":1,"resource":{"primary":{"URL":"https:\/\/rupress.org\/jem\/article\/167\/3\/741\/24050\/The-lpr-gene-causes-an-intrinsic-T-cell"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1988,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1988,3,1]]}},"URL":"https:\/\/doi.org\/10.1084\/jem.167.3.741","relation":{},"ISSN":["0022-1007","1540-9538"],"issn-type":[{"value":"0022-1007","type":"print"},{"value":"1540-9538","type":"electronic"}],"subject":[],"published":{"date-parts":[[1988,3,1]]}}}