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J. Exp. Med.,
Volume 188, Number 6, September 21, 1998 1147-1157
By
From the Immunobiology Program, Department of Medicine, The University of Vermont College of
Medicine, Burlington, Vermont 05405
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)-restricted ovalbumin-specific T cell antigen receptor (TCR) transgenic mice to demonstrate that after in vivo activation with antigen the emergence of
CD4
CD8B220+ 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-restricted TCR. The findings
show that CD4CD8B220+ 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.
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