International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 26(1), P. 70 - 70
Published: Dec. 25, 2024
Paraneoplastic cerebellar degeneration (PCD) is a rapidly progressive, immune-mediated syndrome characterized by the of Purkinje cells, often associated with presence antibodies targeting intracellular antigens within these cells. These autoantibodies are implicated in induction cytotoxicity, leading to cell death, as demonstrated vitro models. However, precise roles and T lymphocytes mediating neuronal injury remain subject ongoing research, cells appearing be main effectors injury. Notably, at least 50% PCD cases involve anti-Yo autoantibodies, also referred anti-PCA1 (Purkinje antigen 1) antibodies, which specifically target degeneration-related protein 2 (CDR2) its paralogue, CDR2-like (CDR2L). Another recognized CDR 34, 34 kDa tandem repeats B-cell epitope; detection non-cerebellar tissues necessitates further situ hybridization studies. Onconeural expressed both tumour where they localize cytoplasm associate membrane-bound free ribosomes, playing critical regulating transcription calcium homeostasis. Recent studies suggest that breakdown immune tolerance linked genetic alterations antigens, formation neoantigens can elicit autoreactive may underscore function Yo antibodies. In indicate induce death independent lymphocytes. The disease progresses initial lymphocytic infiltration, followed rapid loss without significant inflammation. vivo models showcase primarily T-cell mediated, serving biomarkers rather than direct death. This review examines mechanisms underlying PCD, focusing on CDR2 CDR2L development their potential role neurons. A comprehensive understanding processes essential for advancing diagnostic, prognostic, therapeutic strategies malignancies.
Language: Английский