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J Neuroimmune Pharmacol ; 7(4): 927-38, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23054369

RESUMO

Animal models and clinical studies have linked the innate and adaptive immune system to the pathology of Parkinson's disease (PD). Despite such progress, the specific immune responses that influence disease progression have eluded investigators. Herein, we assessed relationships between T cell phenotype and function with PD progression. Peripheral blood lymphocytes from two separate cohorts, a discovery cohort and a validation cohort, totaling 113 PD patients and 96 age- and environment-matched caregivers were examined by flow cytometric analysis and T cell proliferation assays. Increased effector/memory T cells (Tem), defined as CD45RO+ and FAS+ CD4+ T cells and decreased CD31+ and α4ß7+ CD4+ T cells were associated with progressive Unified Parkinson's Disease Rating Scale III scores. However, no associations were seen between immune biomarkers and increased age or disease duration. Impaired abilities of regulatory T cells (Treg) from PD patients to suppress effector T cell function was observed. These data support the concept that chronic immune stimulation, notably Tem activation and Treg dysfunction is linked to PD pathobiology and disease severity, but not disease duration. The association of T cell phenotypes with motor symptoms provides fresh avenues for novel biomarkers and therapeutic designs.


Assuntos
Linfócitos T CD4-Positivos/patologia , Transtornos dos Movimentos/patologia , Doença de Parkinson/patologia , Subpopulações de Linfócitos T/patologia , Contagem de Células Sanguíneas , Linfócitos T CD4-Positivos/metabolismo , Estudos de Coortes , Biologia Computacional , Citometria de Fluxo , Expressão Gênica/fisiologia , Humanos , Interleucina-6/biossíntese , Interleucina-9/biossíntese , Monócitos/patologia , Transtornos dos Movimentos/etiologia , Transtornos dos Movimentos/metabolismo , Doença de Parkinson/genética , Doença de Parkinson/metabolismo , Fenótipo , Subpopulações de Linfócitos T/metabolismo , Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
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