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Department of Molecular Microbiology and Immunology, University of Southern California/Norris Comprehensive Cancer Center, Keck School of Medicine at University of Southern California, Los Angeles, CA 90089
Immunity to allogeneic MHC Ags is weak in rodent livers, raising
questions as to the mechanisms that might control responses in this
organ. Infection with an adenovirus vector reveals that T cell-mediated
immunity to nonself-Ags in the liver is self-limiting. Virus-induced
liver injury decreases and coincides with disappearance of
virus-specific CTL, concomitant to an increase of apoptotic T cells
early after infection. But whereas death in CD4 cells is independent of
Fas, perforin, and TNF-
, that of CD8 cells requires Fas and not
perforin or TNF- pathways. Fas ligand is expressed on
liver-infiltrating cells, pointing to death by fratricide that causes
almost complete disappearance of virus-specific CTL 4 wk after
infection. CTL elimination is virus dose dependent, and high doses
induced high alanine aminotransferase values, elevated expression of
Fas ligand on CD8 cells, and increased CD8 cell migration into the
infected liver.
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