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Science  16 Jan 2009:
Vol. 323, Issue 5912, pp. 311
DOI: 10.1126/science.323.5912.311b

In degenerative disorders of the central nervous system, inflammation at the site of neuronal injury is common, but it has not been clear whether this reaction is a primary factor in subsequent disease pathogenesis or a secondary response to the condition. Brochard et al. report that a particular subpopulation of T cells is critical for the development of Parkinson's disease (PD), a disorder characterized by the loss of brain neurons that use dopamine. The authors report the accumulation of CD4+ and CD8+ T cells in the postmortem brains of PD patients and also in the brains of a mouse model of PD during progression of the disease. However, in mice lacking CD4+ T cells that express the cell surface protein FasL, dopaminergic neuronal injury was reduced, as was the activation of proinflammatory migroglial cells in the brain. FasL could either mediate the activation of microglial cells, thereby promoting inflammation and neurodegeneration, or it could mediate cell-cell contact that somehow allows T cells to destroy neurons directly. — LC

J. Clin. Invest. 119, 182 (2009).

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