Immunopathology of optic neuritis and cerebrospinal fluid biomarkers for acute attack and relapse prediction.

IF 3 4区 医学 Q3 CELL BIOLOGY
Rong Jin, Shihao Sun, Xiangyi Liu, Qing Ge
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Abstract

Optic neuritis (ON), characterized by inflammation and demyelination of the optic nerve, is a leading cause of vision impairment. It frequently manifests as the initial symptom and a recurrent syndrome in patients with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS). While the diagnosis of ON is relatively straightforward, predicting relapses and managing the disease remain significant challenges. The myelination of retinal ganglion cell axons is essential for the efficient and accurate transmission of signals between optic neurons. Oligodendrocytes, specialized glial cells responsible for myelination, engage in metabolic interactions with neurons. Demyelination and inflammation of the optic nerve locally release a variety of metabolites and inflammatory factors within this unique anatomical region. Cerebrospinal fluid (CSF), in close proximity to ON lesions, is a critical source for identifying metabolic and inflammatory biomarkers that are essential for tracking disease activity and guiding therapeutic decisions. This comprehensive review examines the structure, myelination and demyelination of the optic nerve, as well as the immunopathological mechanisms underlying ON. It also explores changes in CSF constituents, including pleocytosis, antibodies, cytokines, proteins, metabolites and extracellular vesicles. Special emphasis is placed on elucidating the pathological contributions of metabolites in MOGAD, MS and NMOSD. By advancing our understanding of these mechanisms, this review elucidates the potential predictive roles of CSF constituents in acute attacks and relapses of optic neuritis.

视神经炎的免疫病理学和脑脊液生物标志物对急性发作和复发的预测。
视神经炎(ON)的特征是视神经的炎症和脱髓鞘,是视力障碍的主要原因。它经常表现为髓鞘少突胶质细胞糖蛋白抗体相关疾病(MOGAD)、视神经脊髓炎谱系障碍(NMOSD)和多发性硬化症(MS)患者的初始症状和复发综合征。虽然ON的诊断相对简单,但预测复发和控制疾病仍然是重大挑战。视网膜神经节细胞轴突的髓鞘形成是视神经细胞之间有效、准确的信号传递所必需的。少突胶质细胞是专门负责髓鞘形成的胶质细胞,参与与神经元的代谢相互作用。视神经脱髓鞘和炎症局部释放多种代谢物和炎症因子在这个独特的解剖区域。脑脊液(CSF)靠近ON病变,是识别代谢和炎症生物标志物的关键来源,这些生物标志物对于跟踪疾病活动和指导治疗决策至关重要。本文综述了视神经的结构、髓鞘形成和脱髓鞘形成,以及视神经病变的免疫病理机制。它还探讨了脑脊液成分的变化,包括多细胞性、抗体、细胞因子、蛋白质、代谢物和细胞外囊泡。特别强调阐明代谢产物在MOGAD, MS和NMOSD中的病理贡献。通过加深我们对这些机制的理解,本综述阐明了脑脊液成分在视神经炎急性发作和复发中的潜在预测作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Immunology & Cell Biology
Immunology & Cell Biology 医学-免疫学
CiteScore
7.50
自引率
2.50%
发文量
98
审稿时长
4-8 weeks
期刊介绍: The Australasian Society for Immunology Incorporated (ASI) was created by the amalgamation in 1991 of the Australian Society for Immunology, formed in 1970, and the New Zealand Society for Immunology, formed in 1975. The aim of the Society is to encourage and support the discipline of immunology in the Australasian region. It is a broadly based Society, embracing clinical and experimental, cellular and molecular immunology in humans and animals. The Society provides a network for the exchange of information and for collaboration within Australia, New Zealand and overseas. ASI members have been prominent in advancing biological and medical research worldwide. We seek to encourage the study of immunology in Australia and New Zealand and are active in introducing young scientists to the discipline.
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