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Institute for Medical Microbiology and Virology, Heinrich Heine University, Duesseldorf, Germany
Microglia subpopulations were studied in mouse experimental
autoimmune encephalomyelitis and toxoplasmic encephalitis. CNS
inflammation was associated with the proliferation of
CD11b+ brain cells that exhibited the dendritic cell (DC)
marker CD11c. These cells constituted up to 30% of the total
CD11b+ brain cell population. In both diseases
CD11c+ brain cells displayed the surface phenotype of
myeloid DC and resided at perivascular and intraparenchymatic
inflammatory sites. By lacking prominent phagocytic organelles,
CD11c+ cells from inflamed brain proved distinct from other
microglia, but strikingly resembled bone marrow-derived DC and thus
were identified as DC. This brain DC population comprised cells
strongly secreting IL-12p70, whereas coisolated CD11c-
microglia/brain macrophages predominantly produced TNF-
, GM-CSF, and
NO. In comparison, the DC were more potent stimulators of naive or
allogeneic T cell proliferation. Both DC and CD11c-
microglia/macrophages from inflamed brain primed naive T cells from
DO11.10 TCR transgenic mice for production of Th1 cytokines IFN-
and
IL-2. Resting microglia that had been purified from normal adult brain
generated immature DC upon exposure to GM-CSF, while CD40 ligation
triggered terminal maturation. Consistently, a functional maturation of
brain DC was observed to occur following the onset of encephalitis. In
conclusion, these findings indicate that in addition to inflammatory
macrophage-like brain cells, intraparenchymatical DC exist in
autoimmune and infectious encephalitis. These DC functionally mature
upon disease onset and can differentiate from resident microglia. Their
emergence, maturation, and prolonged activity within the brain might
contribute to the chronicity of intracerebral Th1
responses.
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