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开发副肿瘤性小脑变性小鼠模型的初步研究。

A Pilot Study to Develop Paraneoplastic Cerebellar Degeneration Mouse Model.

作者信息

Faure Fabrice, Yshii Lidia, Renno Toufic, Coste Isabelle, Joubert Bastien, Desestret Virginie, Liblau Roland, Honnorat Jérôme

机构信息

Synaptopathies and Autoantibodies (SynatAc) Team, Institut NeuroMyoGène (INMG)-MeLis, INSERM U1314, CNRS UMR 5284, Université de Lyon, Université Claude Bernard Lyon 1, 69373, Lyon, France.

Toulouse Institute for Infectious and Inflammatory Diseases (Infinity), University of Toulouse, CNRS, INSERM, UPS, 31024, Toulouse, France.

出版信息

Cerebellum. 2024 Feb;23(1):181-196. doi: 10.1007/s12311-023-01524-6. Epub 2023 Feb 2.

Abstract

Modeling paraneoplastic neurological diseases to understand the immune mechanisms leading to neuronal death is a major challenge given the rarity and terminal access of patients' autopsies. Here, we present a pilot study aiming at modeling paraneoplastic cerebellar degeneration with Yo autoantibodies (Yo-PCD). Female mice were implanted with an ovarian carcinoma cell line expressing CDR2 and CDR2L, the known antigens recognized by anti-Yo antibodies. To boost the immune response, we also immunized the mice by injecting antigens with diverse adjuvants and immune checkpoint inhibitors. Ataxia and gait instability were assessed in treated mice as well as autoantibody levels, Purkinje cell density, and immune infiltration in the cerebellum. We observed the production of anti-Yo antibodies in the CSF and serum of all immunized mice. Brain immunoreaction varied depending on the site of implantation of the tumor, with subcutaneous administration leading to a massive infiltration of immune cells in the meningeal spaces, choroid plexus, and cerebellar parenchyma. However, we did not observe massive Purkinje cell death nor any motor impairments in any of the experimental groups. Self-sustained neuro-inflammation might require a longer time to build up in our model. Unusual tumor antigen presentation and/or intrinsic, species-specific factors required for pro-inflammatory engagement in the brain may also constitute strong limitations to achieve massive recruitment of antigen-specific T-cells and killing of antigen-expressing neurons in this mouse model.

摘要

鉴于患者尸检的罕见性和终末期可及性,建立副肿瘤性神经系统疾病模型以了解导致神经元死亡的免疫机制是一项重大挑战。在此,我们展示了一项旨在建立抗Yo抗体介导的副肿瘤性小脑变性(Yo-PCD)模型的初步研究。给雌性小鼠植入表达CDR2和CDR2L的卵巢癌细胞系,这两种抗原是抗Yo抗体识别的已知抗原。为增强免疫反应,我们还通过注射含有不同佐剂和免疫检查点抑制剂的抗原对小鼠进行免疫。对治疗后的小鼠评估共济失调和步态不稳情况,以及自身抗体水平、浦肯野细胞密度和小脑的免疫浸润情况。我们在所有免疫小鼠的脑脊液和血清中观察到抗Yo抗体的产生。脑免疫反应因肿瘤植入部位而异,皮下给药导致免疫细胞大量浸润脑膜间隙、脉络丛和小脑实质。然而,我们在任何实验组中均未观察到大量浦肯野细胞死亡或任何运动障碍。在我们的模型中,持续性神经炎症可能需要更长时间才能形成。异常的肿瘤抗原呈递和/或大脑中促炎反应所需的内在物种特异性因素,也可能是该小鼠模型中实现抗原特异性T细胞大量募集和杀死表达抗原的神经元的强大限制因素。

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