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Departments of
*
Neurology,
Pathology, and
Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033
CD8+ T cells are required to control acute viral
replication in the CNS following infection with neurotropic
coronavirus. By contrast, studies in B cell-deficient (µMT) mice
revealed Abs as key effectors in suppressing virus recrudescence. The
apparent loss of initial T cell-mediated immune control in the absence
of B cells was investigated by comparing T cell populations in CNS
mononuclear cells from infected µMT and wild-type mice. Following
viral recrudescence in µMT mice, total CD8+ T cell
numbers were similar to those of wild-type mice that had cleared
infectious virus; however, virus-specific T cells were reduced at least
3-fold by class I tetramer and IFN-
ELISPOT analysis. Although
overall T cell recruitment into the CNS of µMT mice was not impaired,
discrepancies in frequencies of virus-specific CD8+ T cells
were most severe during acute infection. Impaired ex vivo cytolytic
activity of µMT CNS mononuclear cells, concomitant with reduced
frequencies, implicated IFN- as the primary anti viral factor early
in infection. Reduced virus-specific CD8+ T cell responses
in the CNS coincided with poor peripheral expansion and diminished
CD4+ T cell help. Thus, in addition to the lack of Ab,
limited CD8+ and CD4+ T cell responses in µMT
mice contribute to the ultimate loss of control of CNS infection. Using
a model of virus infection restricted to the CNS, the results provide
novel evidence for a role of B cells in regulating T cell expansion and
differentiation into effector cells.
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