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Departments of Microbiology-Immunology and Pathology, Northwestern University Medical School, Chicago, IL 60611
Intracerebral inoculation of Theiler’s murine encephalomyelitis
virus (TMEV) into susceptible mouse strains results in a chronic,
immune-mediated demyelinating disease similar to human multiple
sclerosis. Here, we examined the role of astrocytes as an APC
population in TMEV-induced demyelination and assessed the potential
consequences of T cell activation following Ag presentation.
IFN-
-pretreated astrocytes were able to process and present all the
predominant T cell epitopes of TMEV to virus-specific T cell
hybridomas, clones, as well as bulk T cells. Despite low levels of
proliferation of T cells due to prostaglandins produced by astrocytes,
such Ag presentation by activated astrocytes induced the production of
IFN-, a representative proinflammatory cytokine, in TMEV-specific Th
cell clones derived from the CNS of virus-infected mice. Furthermore,
these Th cell clones mediate lysis of the astrocytes in vitro in a
Fas-dependent mechanism. TUNEL staining of CNS tissue demonstrates the
presence of apoptotic GFAP+ cells in the white matter of
TMEV-infected mice. These results strongly suggest that astrocytes
could play an important role in the pathogenesis of TMEV-induced
demyelination by activating T cells, subsequently leading to T
cell-mediated apoptosis of astrocytes and thereby compromising the
blood-brain barrier.
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