Journal
JOURNAL OF IMMUNOLOGY
Volume 167, Issue 3, Pages 1575-1583Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.167.3.1575
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- NIAID NIH HHS [AI 33314] Funding Source: Medline
- NINDS NIH HHS [NS 18146] Funding Source: Medline
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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 (mu MT) 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 mu MT and wild-type mice. Following viral recrudescence in mu MT 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 Mold by class I tetramer and IFN-gamma ELISPOT analysis. Although overall T cell recruitment into the CNS of mu MT 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 mu MT CNS mononuclear cells, concomitant with reduced frequencies, implicated IFN-gamma 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 Ali, limited CD8(+) and CD4(+) T cell responses in mu MT 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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