作者: Hans-Georg Fischer , Gaby Reichmann
DOI: 10.4049/JIMMUNOL.166.4.2717
关键词: Biology 、 T cell 、 CD11c 、 Experimental autoimmune encephalomyelitis 、 Dendritic cell 、 Infectious encephalitis 、 Immunology 、 Central nervous system 、 Microglia 、 Neuroinflammation
摘要: 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 dendritic cell (DC) marker CD11c. These constituted up to 30% total population. In both diseases CD11c displayed surface phenotype myeloid DC resided at perivascular intraparenchymatic inflammatory sites. By lacking prominent phagocytic organelles, from inflamed proved distinct other microglia, but strikingly resembled bone marrow-derived thus identified as DC. This population comprised strongly secreting IL-12p70, whereas coisolated − microglia/brain macrophages predominantly produced TNF-α, GM-CSF, NO. comparison, more potent stimulators naive or allogeneic T proliferation. Both microglia/macrophages primed DO11.10 TCR transgenic mice for production Th1 cytokines IFN-γ IL-2. Resting microglia had been purified normal adult generated immature upon exposure while CD40 ligation triggered terminal maturation. Consistently, a functional maturation observed occur following onset conclusion, these findings indicate addition macrophage-like cells, intraparenchymatical exist infectious functionally mature disease can differentiate resident microglia. Their emergence, maturation, prolonged activity within might contribute chronicity intracerebral responses.