Evidence for a role of adaptive immune response in the disease pathogenesis of the @entity5212 @entity19 model of XXXX .

@entity1 @entity5212 @entity19 @entity5 @entity635 @entity8200 @entity191 @entity179
UNASSIGNED: @entity191 ( @entity191 ) is the second most common @entity179 and results from the loss of dopaminergic neurons of the nigrostriatal pathway. The pathogenesis of @entity191 is poorly understood, but inflammatory processes have been implicated. Indeed increases in the number of major histocompatibility complex II ( @entity8200 ) reactive cells have long been recognised in the brains of @entity191 @entity1 at post-mortem. However whether cells expressing @entity8200 play an active role in @entity191 pathogenesis has not been delineated. This was addressed utilising a transgenic @entity19 null for @entity8200 and the parkinsonian toxin @entity5212 ( @entity5212 ). In wild-type @entity19 @entity8200 levels in the ventral midbrain were upregulated 1-2 days after @entity5212 treatment and @entity8200 was localized in both astrocytes and microglia. @entity8200 null @entity19 showed significant reductions in @entity5212 -induced dopaminergic neuron loss and a significantly reduced invasion of astrocytes and microglia in @entity8200 null @entity19 receiving @entity5212 compared with controls. In addition, @entity8200 null @entity19 failed to show increases in interferon-y or @entity5 necrosis factor-a in the brain after @entity5212 treatment, as was found in wild-type @entity19 . However, @entity635 was significantly increased in both wild-type and @entity8200 null @entity19 . These data indicate that in addition to microglial cell/myeloid cell activation MHC Class II-mediated T cell activation is required for the full expression of pathology in this model of @entity191 . GLIA 2015.
