Coexpression of Fas/FasL and Bax on brain and infiltrating T cells in the central nervous system is closely associated with apoptotic cell death during autoimmune encephalomyelitis
T. Kohji et Y. Matsumoto, Coexpression of Fas/FasL and Bax on brain and infiltrating T cells in the central nervous system is closely associated with apoptotic cell death during autoimmune encephalomyelitis, J NEUROIMM, 106(1-2), 2000, pp. 165-171
Recent studies have suggested that autoimmune inflammation elicited in the
central nervous system (CNS) is subsided by apoptotic cell death of inflamm
atory cells. To elucidate the molecular mechanism of apoptosis of infiltrat
ing T and other cells occurring in the CNS during autoimmune encephalomyeli
tis, we determined the type of apoptotic cells and the localization of apop
tosis-related molecules (Fas, FasL, Bax, Bcl-2 and active caspase 3) by imm
unohistochemistry. Double labeling with the TUNEL method and cell-type mark
ers showed that infiltrating T cells and microglia/macrophages underwent ap
optosis, while astrocytes and neurons did not. Staining for apoptosis-relat
ed molecules revealed that infiltrating T cells and microglia/macrophages,
but not astrocytes and neurons, expressed both Fas-FasL and Bax. The distri
bution and cell type of active caspase 3-positive cells were essentially th
e same as those of TUNEL-positive cells. These findings suggest that coexpr
ession of Fas/FasL and Bax is closely associated with apoptotic cell death
of infiltrating T cells and microglia in the CNS. Furthermore, astrocytes w
hich express Fas and FasL, but not Bax, may play an important role in regul
ating inflammation in the CNS by inducing apoptotic cell death of infiltrat
ing T cells and microglia, both of which have an inflammation-promoting nat
ure. (C) 2000 Elsevier Science B.V. All rights reserved.