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CDR2和CDR2L在抗Yo副肿瘤性小脑变性中的作用:文献综述

Roles of CDR2 and CDR2L in Anti-Yo Paraneoplastic Cerebellar Degeneration: A Literature Review.

作者信息

Martínez Lozada Pablo S, Mancero Montalvo Rafael, Iturralde Carrillo Andrea, Montesdeoca-Lozada Maria, Rodas Jose A, Leon-Rojas Jose E

机构信息

NeurALL Research Group, Quito 170157, Ecuador.

Medical School, Universidad Internacional del Ecuador (UIDE), Quito 170411, Ecuador.

出版信息

Int J Mol Sci. 2024 Dec 25;26(1):70. doi: 10.3390/ijms26010070.

Abstract

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

摘要

副肿瘤性小脑变性(PCD)是一种快速进展的免疫介导综合征,其特征为浦肯野细胞变性,常与靶向这些细胞内细胞抗原的抗体的存在相关。如体外模型所示,这些自身抗体参与细胞毒性的诱导,导致浦肯野细胞死亡。然而,抗体和T淋巴细胞在介导神经元损伤中的精确作用仍是一个正在进行研究的课题,T细胞似乎是小脑损伤的主要效应细胞。值得注意的是,至少50%的PCD病例涉及抗Yo自身抗体,也称为抗PCA1(浦肯野细胞抗原1)抗体,其特异性靶向小脑变性相关蛋白2(CDR2)及其旁系同源物CDR2样蛋白(CDR2L)。另一种公认的抗原是CDR 34,一种34 kDa的浦肯野细胞抗原,其特征为串联重复序列和一个B细胞表位;在非小脑组织中检测到它需要进一步的原位杂交研究。肿瘤神经抗原在浦肯野细胞和肿瘤细胞中均有表达,它们定位于细胞质中,并与膜结合核糖体和游离核糖体相关联,在调节转录和钙稳态中发挥关键作用。最近的研究表明,免疫耐受的破坏与肿瘤细胞抗原的基因改变有关,导致新抗原的形成,这些新抗原可引发自身反应性T细胞,这可能突出了Yo抗体的功能。体外研究表明,抗Yo抗体可独立于T淋巴细胞诱导细胞死亡。该疾病最初通过淋巴细胞浸润进展,随后浦肯野细胞迅速丢失,且无明显炎症。然而,体内模型显示抗Yo PCD主要由T细胞介导,抗体作为生物标志物而非神经元死亡的直接效应物。本综述探讨了PCD的潜在机制,重点关注CDR2和CDR2L在肿瘤发生中的作用及其在小脑浦肯野神经元变性中的潜在作用。全面了解这些过程对于推进PCD及相关恶性肿瘤的诊断、预后和治疗策略至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b48/11720089/75b3c650c5e0/ijms-26-00070-g001.jpg

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