dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorPacheco, Rodrigo
dc.date.accessioned2023-05-24T01:10:53Z
dc.date.available2023-05-24T01:10:53Z
dc.date.created2023-05-24T01:10:53Z
dc.date.issued2021
dc.identifierhttps://repositorio.uss.cl/handle/uss/1985
dc.identifier10.37349/ent.2021.00007
dc.description.abstractCurrent evidence indicates that neurodegeneration of dopaminergic neurons of the substantia nigra associated to Parkinson’s disease is a consequence of a neuroinflammatory process in which microglial cells play a central role. The initial activation of microglial cells is triggered by pathogenic protein inclusions, which are mainly composed by α-synuclein. Importantly, these pathogenic forms of α-synuclein subsequently induce a T-cell-mediated autoimmune response to dopaminergic neurons. Depending on their functional phenotype, these autoreactive T-cells might shape the functional features of activated microglia. T-cells bearing pro-inflammatory phenotypes such as T-helper (Th)1 or Th17 promote a chronic inflammatory behaviour on microglia, whilst anti-inflammatory T-cells, such as regulatory T-cells (Treg) favour the acquisition of neuroprotective features by microglia. Thus, T-cells play a fundamental role in the development of neuroinflammation and neurodegeneration involved in Parkinson’s disease. This review summarizes the evidence indicating that not only CD4+ T-cells, but also CD8+ T-cells play an important role in the physiopathology of Parkinson’s disease. Next, this review analyses the different T-cell epitopes derived from the pathogenic forms of α-synuclein involved in the autoimmune response associated to Parkinson’s disease in animal models and humans. It also summarizes the requirement of specific alleles of major histocompatibility complexes (MHC) class I and class II necessaries for the presentation of CD8+ and CD4+ T-cell epitopes from the pathogenic forms of α-synuclein in both humans and animal models. Finally, this work summarizes and discusses a number of experimental immunotherapies that aim to strengthen the Treg response or to dampen the inflammatory T-cell response as a therapeutic approach in animal models of Parkinson’s disease.
dc.languagespa
dc.relationExploration of Neuroprotective Therapy
dc.titleT-cell based immunotherapies for Parkinson’s disease
dc.typeArtículo


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