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*
Institute for Medical Microbiology and Virology, Heinrich-Heine University, Duesseldorf, Germany; and
Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104
During chronic infection of mice with Toxoplasma
gondii, gene message for IL-12p40, CD86, and the potassium
channel Kv1.3 was detected in brain mononuclear cells, suggesting the
presence of dendritic cells (DC) in the CNS. Consistently, cells
bearing the DC markers CD11c and 33D1 were localized at inflammatory
sites in the infected brain. The number of isolated CD11c+
brain cells increased until peak inflammation. The cells exhibited the
surface phenotype of myeloid DC by coexpressing 33D1 and F4/80, little
DEC-205, and no CD8
. These brain DC were mature, as indicated by
high-level expression of MHC class II, CD40, CD54, CD80, and CD86. They
triggered Ag-specific and primary allogeneic T cell responses at very
low APC/T cell ratios. Among mononuclear cells from encephalitic brain,
DC were the main producers of IL-12. Evidence for a parasite-dependent
development of DC from CNS progenitors was obtained in vitro: after
inoculation of primary brain cell culture with T.
gondii, IL-12-secreting dendriform cells emerged, and DC marker
genes were expressed. Different stimuli elicited the generation and
maturation of brain DC: neutralization of parasite-induced GM-CSF
prevented outgrowth of dendriform cells and concomitant release of
IL-12. IL-12 production was up-regulated by external IFN-
but was
stopped by inhibiting parasite replication. Consistently, DC isolated
from GM-CSF-treated brain cell culture were activated to secrete IL-12
by exposure to parasite lysate. In sum, these results demonstrate
T. gondii-induced expansion and functional maturation of
DC in the CNS and, thus, highlight a mechanism that may contribute to
the chronicity of the host response.
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