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*
Laboratory of Tumor Immunology, Division of Oncology, and
Department of Neurosurgery, University Hospital, Geneva, Switzerland; and
Laboratory of Immunopathology, Faculty of Medicine, Marseille, France
Astrocytes are a major cellular component of the brain that are
capable of intense proliferation and metabolic activity during diverse
inflammatory brain diseases (such as multiple sclerosis, Alzheimer’s
dementia, tumor, HIV encephalitis, or prion disease). In this
biological process, called reactive gliosis, astrocyte apoptosis is
frequently observed and could be an important mechanism of regulation.
However, the factors responsible for apoptosis in human astrocytes are
poorly defined. Here, we report that short term cultured astrocytes
derived from different brain regions express significant levels of CD95
at their surface. Only late passage astrocytes are sensitive to CD95
ligation using either CD95 mAb or recombinant CD95 ligand. Blocking
experiments using caspase inhibitors with different specificities
(DEVD-CHO, z-VAD-fmk, and YVAD-cmk), an enzymatic activity assay, and
immunoblotting show that CPP32/caspase-3 play a prominent role in
CD95-induced astrocyte death. In contrast, early passage astrocytes are
totally resistant to death, but a significant increase in astrocytic
IL-8 secretion (p < 0.001, by Wilcoxon’s test for
paired samples) is observed after CD95 triggering. Production of IL-8
contributes to the resistance of astrocytes to CD95 ligation.
Furthermore, in the presence of IFN-
, resistant astrocytes became
sensitive to CD95-mediated death. These data suggest that
microenvironmental factors can influence the consequences of CD95
ligation on astrocytes. Therefore, we propose that CD95 expressed by
human astrocytes plays a pivotal role in the regulation of astrocyte
life and death and may be a key factor in inflammatory processes in the
brain, such as reactive gliosis.
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