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本文引用的文献
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Th17 Lymphocytes Induce Neuronal Cell Death in a Human iPSC-Based Model of Parkinson's Disease.
Cell Stem Cell. 2018 Jul 5;23(1):123-131.e6. doi: 10.1016/j.stem.2018.06.015.
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T cells from patients with Parkinson's disease recognize α-synuclein peptides.
Nature. 2017 Jun 29;546(7660):656-661. doi: 10.1038/nature22815. Epub 2017 Jun 21.
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Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson's Disease.
Cell. 2016 Dec 1;167(6):1469-1480.e12. doi: 10.1016/j.cell.2016.11.018.
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Th17 Cells Induce Dopaminergic Neuronal Death via LFA-1/ICAM-1 Interaction in a Mouse Model of Parkinson's Disease.
Mol Neurobiol. 2017 Dec;54(10):7762-7776. doi: 10.1007/s12035-016-0249-9. Epub 2016 Nov 14.
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MHC-I expression renders catecholaminergic neurons susceptible to T-cell-mediated degeneration.
Nat Commun. 2014 Apr 16;5:3633. doi: 10.1038/ncomms4633.
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The role of innate and adaptive immunity in Parkinson's disease.
J Parkinsons Dis. 2013;3(4):493-514. doi: 10.3233/JPD-130250.
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MHCII is required for α-synuclein-induced activation of microglia, CD4 T cell proliferation, and dopaminergic neurodegeneration.
J Neurosci. 2013 Jun 5;33(23):9592-600. doi: 10.1523/JNEUROSCI.5610-12.2013.
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Common genetic variation in the HLA region is associated with late-onset sporadic Parkinson's disease.
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Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease.
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