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* Institut für Medizinische Mikrobiologie und Hygiene, Universitätsklinikum Mannheim, Universität Heidelberg, Mannheim, Germany; and
Abteilung für Neuropathologie, Klinikum der Universität zu Köln, Cologne, Germany
The invasion of the CNS by pathogens poses a major risk for damage
of the highly vulnerable brain. The aim of the present study was to
analyze immunological mechanisms that may prevent spread of infections
to the CNS. Intraperitoneal application of Listeria
monocytogenes to mice induced infection of the spleen, whereas
pathogens remained absent from the brain. Interestingly,
Listeria-specific CD4 and CD8 T cells homed to the brain
and persisted intracerebrally for at least 50 days after both primary
and secondary infection. CD4 and CD8 T cells resided in the
leptomeninges, in the choroid plexus, and, in low numbers, in the brain
parenchyma. CD4 and CD8 T cells isolated from the brain early after
infection (day 7) were characterized by an activated phenotype with
spontaneous IFN-
production, whereas at a later stage of infection
(day 28) restimulation with Listeria-specific peptides
was required for the induction of IFN- production by CD4 and CD8 T
cells. In contrast to splenic T cells, T cells in the brain did not
exhibit cytotoxic activity. Adoptively transferred T cells isolated
from the brains of Listeria-infected mice reduced the
bacterial load in cerebral listeriosis. The frequency of intracerebral
Listeria-specific T cells was partially regulated by the
time of exposure to Listeria and cross-regulated by CD4
and CD8 T cells. Collectively, these data reveal a novel T
cell-mediated pathway of active immunosurveillance of the CNS during
bacterial infections.
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