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-Irradiation in B6 and B6/lpr Mice1
Departments of
*
Medicine and
Microbiology/Immunology, University of North Carolina, Chapel Hill, NC 27599
Fas (CD95) is a cell surface protein that mediates apoptosis.
lpr is a mutation of the Fas gene caused by a retroviral
insertion resulting in premature termination of transcription and
aberrant splicing of Fas mRNA. Mice homozygous for the
lpr gene develop lymphoproliferation and produce
autoantibodies closely resembling those of human systemic lupus
erythematosus. While lpr mice have been reported to
express low levels of normally spliced Fas mRNA, it is unknown whether
they express functional Fas protein. Here we show that splenocytes from
lpr mice that have been damaged by 
-irradiation
expressed Fas protein. Fas was up-regulated on irradiated B6 cells and
could be detected on B6/lpr cells undergoing apoptosis
following in vitro culture. Detection of Fas on live lpr
cells was demonstrable when apoptosis was blocked by zinc. In a short
term chimera system, Fas was shown to play a role, in vivo, in the
disposition of radiation-injured cells from both normal and
lpr mice. The addition of anti-Fas Ab to in vitro
cultures resulted in an increase in apoptosis in both B6 and
B6/lpr cells. Detection of intact Fas message and low
levels of Fas protein in lpr mice has led to the
consideration of lpr as a leaky mutation. This study
demonstrates that lpr mice can produce functional Fas
protein. This system is also appropriate for identifying the in vivo
role of Fas/FasL in apoptosis following other cell
manipulations.
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