This research explores how B cells contribute to the development of multiple sclerosis (MS) by interacting with the Epstein-Barr virus (EBV). The study demonstrates that B cells can capture myelin antigens and present them to T cells, a process that triggers inflammation within the central nervous system. By using mouse models, the authors show that expressing the EBV protein LMP1 allows autoreactive B cells to survive and expand rather than undergoing typical cell death. Findings also indicate that blood-brain barrier disruptions from past infections may facilitate the entry of these harmful cells into the brain. Ultimately, the paper suggests that EBV-induced survival of self-reactive B cells is a primary driver of demyelination. These insights support the potential for EBV vaccines or targeted therapies to prevent or treat the disease.

References:

• Kim H, Schneider M, Raach Y, et al. Myelin antigen capture in the CNS by B cells expressing EBV latent membrane protein 1 leads to demyelinating lesion formation[J]. Cell, 2026.