Immune response profiling of HERV-W envelope proteins in multiple sclerosis: potential biomarkers for disease progression

多发性硬化症中HERV-W包膜蛋白的免疫反应谱分析:疾病进展的潜在生物标志物

阅读:3

Abstract

INTRODUCTION: The envelope proteins syncytin-1 and pHERV-W from the Human Endogenous Retroviral family 'W' (HERV-W) have been identified as potential risk factors in multiple sclerosis (MS). This study aims to evaluate both humoral and cell-mediated immune response to antigenic peptides derived from these proteins across different clinical forms and inflammatory phases of MS. METHODS: Indirect enzyme-linked immunosorbent assay (ELISA) was employed to measure immunoglobulin G (IgG) responses to syncytin-1(env 486-500) and pHERV-W(env 486-504) peptides in MS patients. Discriminant analysis was used to assess whether clinical course prediction could be enhanced by integrating clinical variables with humoral response data against other MS-associated viral factors. Additionally, peripheral blood mononuclear cells from MS patients and healthy controls (HC) were analyzed for inflammatory responses following stimulation with these peptides. RESULTS: MS patients exhibited significantly elevated antibody titers against -pHERV-W(env 486-504) and syncytin-1(env 486-500) compared to HCs, with the highest levels observed in progressive MS forms. Discriminant analysis accurately predicted the clinical course in 75.3% of the cases, with an 85% accuracy rate for progressive MS. In vitro, stimulation with pHERV-W(env 486-504) led to a notable increase in pro-inflammatory cytokine production by CD4, CD8, and CD19 cells compared to syncytin-1(env 486-500). (A) strong correlation was found between pHERV- W(env 486-504) induced cytokine production and EBV and CMV titers in MS patients. DISCUSSION: These findings suggest that the pHERV-W envelope protein could be a valuable biomarker for monitoring peripheral inflammation in MS.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。