DNA methylation and B cells in multiple sclerosis research

MS Breakthrough: Can DNA Methylation Unlock New Treatments?

Beau Callahan in Health & Wellness August 2025 • 4 min read.

"Groundbreaking research identifies potential epigenetic targets for multiple sclerosis therapies, offering hope for personalized medicine."

Multiple sclerosis (MS) is a chronic, debilitating disease where the immune system attacks the central nervous system, leading to a range of neurological problems. While current treatments can help manage the symptoms and slow the progression, there's no cure, and scientists are constantly searching for new ways to understand and combat this complex condition.

A recent study published in Scientific Reports sheds light on a promising area of research: epigenetics and, specifically, DNA methylation. Epigenetics refers to changes in gene expression that don't involve alterations to the DNA sequence itself. DNA methylation, a key epigenetic mechanism, plays a crucial role in regulating gene activity and may be influenced by both genetic and environmental factors.

This article delves into the findings of this study, exploring how DNA methylation patterns in specific immune cells (B cells) differ between MS patients and healthy individuals. We'll uncover the potential implications of these differences for MS risk, treatment response, and the development of innovative therapeutic strategies.

Decoding DNA Methylation in MS: A New Target?

DNA methylation and B cells in multiple sclerosis research

The study focused on CD19+ B cells, a type of immune cell that plays a significant role in the inflammatory processes in MS. Researchers compared the DNA methylation patterns of these cells in 24 patients with relapsing-remitting MS (RRMS) to 24 healthy controls. Using advanced genomic technologies, they identified regions of the genome where DNA methylation differed significantly between the two groups.

The most striking finding was a large differentially methylated region (DMR) at the lymphotoxin-alpha (LTA) locus. This region was hypermethylated in MS patients, meaning there was an increased level of DNA methylation compared to the healthy controls. This is important because LTA encodes for lymphotoxin-alpha (LT-α), a pro-inflammatory cytokine implicated in the development of MS.

LTA's Role: LT-α is overexpressed in various immune cells of MS patients, contributing to inflammation and demyelination (damage to the protective covering of nerve fibers).
Hypermethylation Implication: Hypermethylation in the LTA region could potentially lead to reduced LTA expression, which might seem counterintuitive given its pro-inflammatory role. However, the relationship between methylation and gene expression is complex, and other factors could be at play.
Potential Therapeutic Avenue: The LTA locus is an interesting potential target for future MS treatments.

The researchers also observed smaller DMRs at four genes previously linked to MS: SLC44A2, LTBR, CARD11, and CXCR5. These findings further support the idea that B-cell specific DNA methylation may be associated with MS risk or response to therapy.

The Future of MS Treatment: Targeting Epigenetics

This study provides valuable insights into the role of DNA methylation in MS, particularly in B cells. The identification of the LTA locus as a major DMR opens new avenues for research and potential therapeutic development. However, it's essential to acknowledge that this is preliminary research, and further investigation is needed to validate these findings and understand their functional significance.

One crucial area for future research is to determine how these methylation changes affect LTA expression and the overall inflammatory process in MS. Additionally, studies are needed to explore the potential of targeting DNA methylation at the LTA locus as a therapeutic strategy.

Epigenetic therapies are gaining increasing attention in various diseases, including cancer and autoimmune disorders. The development of B-cell specific epigenetic therapies could represent a paradigm shift in MS treatment, offering a more targeted and personalized approach to managing this complex condition.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1038/s41598-018-35603-0, Alternate LINK

Title: Genome-Wide Dna Methylation Changes In Cd19+ B Cells From Relapsing-Remitting Multiple Sclerosis Patients

Subject: Multidisciplinary

Journal: Scientific Reports

Publisher: Springer Science and Business Media LLC

Authors: Vicki E. Maltby, Rodney A. Lea, Moira C. Graves, Katherine A. Sanders, Miles C. Benton, Lotti Tajouri, Rodney J. Scott, Jeannette Lechner-Scott

Published: 2018-11-27

Everything You Need To Know

What is DNA methylation, and how is it relevant to multiple sclerosis research?

DNA methylation is an epigenetic mechanism that regulates gene activity without changing the DNA sequence itself. In multiple sclerosis research, alterations in DNA methylation patterns, particularly in immune cells like B cells, have been identified. These changes can influence the expression of genes involved in the disease's progression, such as those at the LTA locus. Understanding these methylation patterns may offer insights into MS risk, treatment response, and potential therapeutic strategies.

Which immune cells were examined in the MS study, and what specific genes showed differences in DNA methylation?

The study focused on CD19+ B cells in patients with relapsing-remitting MS (RRMS). Researchers examined the DNA methylation patterns of these cells and compared them to those of healthy individuals. They identified regions in the genome, specifically at the lymphotoxin-alpha (LTA) locus and genes like SLC44A2, LTBR, CARD11, and CXCR5, where DNA methylation differed significantly between the two groups.

What is the significance of the LTA locus in the context of multiple sclerosis?

The LTA locus, which encodes for lymphotoxin-alpha (LT-α), showed a significant difference in DNA methylation between MS patients and healthy controls. Specifically, the LTA region was hypermethylated in MS patients. Since LT-α is a pro-inflammatory cytokine implicated in the development of MS, understanding this hypermethylation could potentially lead to new therapeutic strategies targeting the inflammatory processes in MS.

What are the implications of hypermethylation in the LTA region for the treatment of MS?

Hypermethylation in the LTA region could lead to reduced LTA expression, which seems counterintuitive since LT-α promotes inflammation in MS. The relationship between methylation and gene expression is intricate, with other factors potentially affecting the ultimate outcome. The LTA locus is a potential target for future MS treatments aimed at modulating the inflammatory response.

How could targeting DNA methylation lead to the development of new treatments for multiple sclerosis?

This research highlights the potential of targeting epigenetic mechanisms, specifically DNA methylation, for MS treatment. By identifying the LTA locus and other genes (SLC44A2, LTBR, CARD11, and CXCR5) with differential methylation patterns, researchers can explore new therapeutic avenues to modify gene expression in immune cells and ultimately combat the disease. Further research is needed to validate these findings and fully understand the functional implications of these methylation changes in MS.