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, or IFN-
Departments of
*
Microbiology and Institute for Immunology and Immunological Diseases,
Neurology, and
Pharmacology, Yonsei University College of Medicine, Seoul, Korea; and
§
Wonju College of Medicine, Yonsei University, Wonju, Korea
Fas ligand (FasL) and Fas are mediators of apoptosis, which are
implicated in the peripheral deletion of autoimmune cells,
activation-induced T cell death, and cytotoxicity mediated by
CD8+ T cells. Fas is also believed to be involved in
several central nervous system diseases, but until now, the effector
cells expressing FasL in the brain have not been identified. We
investigated the expression levels of Fas and FasL with the stimulation
of cytokines and the possible effector cells targeting Fas-bearing
cells. Our data demonstrated that: 1) FasL is expressed constitutively
on astrocytes taken from a fetus or an adult and that its expression
increases when these cells are treated with IL-1, IL-6, or TNF-
in
which the pretreatment of IFN-
triggers astrocytes to express more
FasL; 2) astrocytes induce apoptosis in MOLT-4 cells through FasL; 3)
Fas is also expressed constitutively and is up-regulated by IL-1, IL-6,
or TNF- in which the pretreatment of IFN- triggers astrocytes to
express more Fas; 4) apoptosis occurs when fetal astrocytes are treated
with agonistic anti-Fas IgM Ab after culture with IFN- and
TNF-; and 5) TNF-related apoptosis inducing ligand is up-regulated
in fetal astrocytes with stimuli of IL-1 or TNF-. These findings
suggest a possible role of astrocytes in the induction of apoptosis in
central nervous system diseases.
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