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Functional studies in the R6/2 mouse model of Huntington's disease showed a reduced capacity for glutamate oxidation (Skotte et al

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It also seems that the redox potential of GSH may increase the activity of thiol proteases essential in antigen processing and the cleaving of invariant chains from major histocompatibility complex class II, the main role of which is presenting processed antigens to CD4(+) T-lymphocytes [74,75]