ORIGINAL RESEARCH article
Front. Neurol.
Sec. Multiple Sclerosis and Neuroimmunology
Volume 16 - 2025 | doi: 10.3389/fneur.2025.1552149
FCRL3 genetic variants drive autoimmune pathogenesis in multiple sclerosis and neuromyelitis optica spectrum disorders
Provisionally accepted
- 1Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China
- 2Department of Neurology, First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian Province, China
- 3Department of Neurology, Huashan Hospital, Fudan University, Shanghai, Shanghai Municipality, China
- 4Centre for Health and Life Sciences, Faculty of Health and Life Sciences, Coventry University, Coventry, West Midlands, United Kingdom
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Objective: This study aims to investigate the association of Fc receptor-like 3 (FCRL3) gene variants with multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) in a Chinese population cohort.: In Stage 1, 154 MS patients, 109 NMOSD patients, and 301 normal controls were recruited, Sequenom MassARRAY technology was used for genotyping single nucleotide polymorphisms (SNPs). Stage 2 involved an independent cohort of 95 MS patients, 139 NMOSD patients, and 226 normal controls. Two FCRL3 SNPs (rs7528684 and rs11264799) were determined using allele-specific polymerase chain reaction (PCR) with specific primers. Results: Allele C of rs7528684 emerged as a protective factor for MS. Allele A of rs11264799 exhibited no significant effect on MS or NMOSD. A notable disparity in rs7528684 genotype distribution was observed between oligoclonal band (OCB)-positive and OCB-negative MS patients. Allele C of rs7528684 exhibited an association with OCB-positive MS patients.The findings suggest that the FCRL3 variant (rs7528684) is associated with MS rather than NMOSD. FCRL3 might significantly contribute to OCB synthesis, while the underlying mechanisms warrant further elucidation.
Keywords: Multiple Sclerosis, neuromyelitis optica spectrum disorders, FCRL3, variant, Association
Received: 27 Dec 2024; Accepted: 19 Jun 2025.
Copyright: © 2025 Huang, Liu, Xu, Zhao, Liu, Yu and Wu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Hao Yu, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, Zhejiang Province, China
Zhi-Ying Wu, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, Zhejiang Province, China
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