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The pathogenesis of PD is poorly understood, but inflammatory processes have been implicated. Indeed increases in the number of major histocompatibility complex II (MHC II) reactive cells have long been recognised in the brains of PD patients at post\u2010mortem. However whether cells expressing MHC II play an active role in PD pathogenesis has not been delineated. This was addressed utilising a transgenic mouse null for MHC II and the parkinsonian toxin 1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine (MPTP). In wild\u2010type mice MHC II levels in the ventral midbrain were upregulated 1\u20132 days after MPTP treatment and MHC II was localized in both astrocytes and microglia. MHC II null mice showed significant reductions in MPTP\u2010induced dopaminergic neuron loss and a significantly reduced invasion of astrocytes and microglia in MHC II null mice receiving MPTP compared with controls. In addition, MHC II null mice failed to show increases in interferon\u2010\u03b3 or tumour necrosis factor\u2010\u03b1 in the brain after MPTP treatment, as was found in wild\u2010type mice. However, interleukin\u20101\u03b2 was significantly increased in both wild\u2010type and MHC II null mice. These data indicate that in addition to microglial cell\/myeloid cell activation MHC Class II\u2010mediated T cell activation is required for the full expression of pathology in this model of PD. 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