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Departments of
*
Cell Biology and
Medicine, University of Alabama at Birmingham, Birmingham, AL 35294
Fas/Apo-1 is a member of the TNF receptor superfamily that signals
apoptotic cell death in susceptible target cells. Fas or Fas ligand
(FasL)-deficient mice are relatively resistant to the induction of
experimental allergic encephalomyelitis, implying the involvement of
Fas/FasL in this disease process. We have examined the regulation and
function of Fas expression in glial cells (astrocytes and microglia).
Fas is constitutively expressed by primary murine microglia at a low
level and significantly up-regulated by TNF-
or IFN-
stimulation.
Primary astrocytes express high constitutive levels of Fas, which are
not further affected by cytokine treatment. In microglia, Fas
expression is regulated at the level of mRNA expression; TNF- and
IFN- induced Fas mRNA by 
20-fold. STAT-1 and NF-
B
activation are involved in IFN-- or TNF--mediated Fas
up-regulation in microglia, respectively. The cytokine TGF-ß inhibits
basal expression of Fas as well as cytokine-mediated Fas expression by
microglia. Upon incubation of microglial cells with FasL-expressing
cells, 20% of cells underwent Fas-mediated cell death, which
increased to 60% when cells were pretreated with either TNF-
or IFN-. TGF-ß treatment inhibited Fas-mediated cell death of
TNF-- or IFN--stimulated microglial cells. In contrast,
astrocytes are resistant to Fas-mediated cell death, however, ligation
of Fas induces expression of the chemokines macrophage inflammatory
protein-1ß (MIP-1ß), MIP-1, and MIP-2. These data demonstrate
that Fas transmits different signals in the two glial cell populations:
a cytotoxic signal in microglia and an inflammatory signal in the
astrocyte.
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