{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T04:47:56Z","timestamp":1770698876301,"version":"3.49.0"},"reference-count":34,"publisher":"Rockefeller University Press","issue":"6","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1998,9,21]]},"abstract":"<jats:p>Little is understood of the anatomical fate of activated T lymphocytes and the consequences they have on the tissues into which they migrate. Previous work has suggested that damaged lymphocytes migrate to the liver. This study compares class I versus class II major histocompatibility complex (MHC)\u2013restricted ovalbumin-specific T cell antigen receptor (TCR) transgenic mice to demonstrate that after in vivo activation with antigen the emergence of CD4\u2212CD8\u2212B220+ T cells occurs more frequently from a CD8+ precursor than from CD4+ T cells. Furthermore, this change in phenotype is conferred only by the high affinity native peptide antigen and not by lower affinity peptide variants. After activation of CD8+ cells with only the high affinity peptide, there is also a dramatically increased number of liver lymphocytes with accompanying extensive hepatocyte damage and elevation of serum aspartate transaminase. This was not observed in mice bearing a class II MHC\u2013restricted TCR. The findings show that CD4\u2212CD8\u2212B220+ T cells preferentially derive from a CD8+ precursor after a high intensity TCR signal. After activation, T cells can migrate to the liver and induce hepatocyte damage, and thereby serve as a model of autoimmune hepatitis.<\/jats:p>","DOI":"10.1084\/jem.188.6.1147","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T16:49:30Z","timestamp":1027702170000},"page":"1147-1157","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":40,"title":["Liver Damage Preferentially Results from CD8+ T Cells Triggered by High Affinity Peptide Antigens"],"prefix":"10.1084","volume":"188","author":[{"given":"Jennifer Q.","family":"Russell","sequence":"first","affiliation":[{"name":"From the Immunobiology Program, Department of Medicine, The University of Vermont College of Medicine, Burlington, Vermont 05405"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gregory J.","family":"Morrissette","sequence":"additional","affiliation":[{"name":"From the Immunobiology Program, Department of 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