This is an interesting paper, ties in alpha synuclein aggregations, microglial activation with CD4 T cells. They also proposed a model for PD. Good work.
Girija

1: J Immunol. 2009 Apr 1;182(7):4137-49.Click here to read Links
Nitrated {alpha}-synuclein-induced alterations in microglial immunity are regulated by CD4+ T cell subsets.
Reynolds AD, Stone DK, Mosley RL, Gendelman HE.

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, 68198, USA.

Microglial inflammatory neuroregulatory activities affect the tempo of nigrostriatal degeneration during Parkinson's disease (PD). Such activities are induced, in part, by misfolded, nitrated alpha-synuclein (N-alpha-syn) within Lewy bodies released from dying or dead dopaminergic neurons. Such pathobiological events initiate innate and adaptive immune responses affecting neurodegeneration. We posit that the neurobiological activities of activated microglia are affected by cell-protein and cell-cell contacts, in that microglial interactions with N-alpha-syn and CD4(+) T cells substantively alter the microglial proteome. This leads to alterations in cell homeostatic functions and disease. CD4(+)CD25(+) regulatory T cells suppress N-alpha-syn microglial-induced reactive oxygen species and NF-kappaB activation by modulating redox-active enzymes, cell migration, phagocytosis, and bioenergetic protein expression and cell function. In contrast, CD4(+)CD25(-) effector T cells exacerbate microglial inflammation and induce putative neurotoxic responses. These data support the importance of adaptive immunity in the regulation of Parkinson's disease-assoc.............