中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (7): 2832-2833.doi: 10.4103/NRR.NRR-D-25-00206

• 观点:退行性病与再生 • 上一篇    

多发性硬化症中脑屏障处抗原呈递

  

  • 出版日期:2026-07-15 发布日期:2025-10-20

Antigen presentation at the brain barriers in multiple sclerosis

Joshua Brands, Jeroen Bogie, Bieke Broux*   

  1. University MS Center, Campus Diepenbeek, Diepenbeek, Belgium (Brands J, Bogie J, Broux B) Neuro-Immune Connections and Repair Lab, Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium (Broux B)
  • Online:2026-07-15 Published:2025-10-20
  • Contact: Bieke Broux, PhD, Bieke.broux@uhasselt.be.
  • Supported by:
    This work was supported by Belgian Charcot Foundation (to BB).

摘要: https://orcid.org/0000-0001-8509-2415 (Bieke Broux)

Abstract: Loss of immune tolerance to central nervous system (CNS) antigens lies at the heart of multiple sclerosis (MS), the most common chronic autoimmune disease of the CNS. MS affects nearly 2 million people worldwide and is characterized by focal areas of demyelination, inflammation, axonal injury, and neurodegeneration (Bronge et al., 2022; Magliozzi et al., 2023). The condition leads to symptoms such as numbness, muscle weakness, fatigue, visual impairment, and cognitive decline (Magliozzi et al., 2023). Although autoreactive T cells are considered to be primed in peripheral lymphoid tissues initially, it is the local reactivation of these T cells upon encountering CNS antigens that critically drives the inflammatory response within the CNS (Koch et al., 2022). It has become increasingly apparent that brain barriers, such as the blood–brain barrier (BBB), the blood– cerebrospinal fluid barrier (BCSFB), and the meninges, are central to modulating the immune response and driving MS pathology, potentially by facilitating antigen presentation and thus T cell reactivation (Ampie and McGavern, 2022; Magliozzi et al., 2023; Zierfuss et al., 2024). In this perspective, we examine current evidence on how antigen presentation occurs at major brain barrier sites and their contribution to triggering MS onset and progression.