Multiple Sclerosis Overview

Multiple sclerosis (MS) is the most common autoimmune demyelinating disease of the central nervous system and a leading cause of non-traumatic neurological disability in young adults. The third edition of the Atlas of MS and subsequent Global Burden of Disease analyses estimate that around 2.8 million people were living with MS worldwide in 2020, with prevalence still rising. The typical age at diagnosis is 20–40 years, and women are roughly twice as likely to be affected as men.

Pathologically, MS lesions show multifocal inflammation, demyelination, axonal transection, neuronal loss and gliosis throughout the brain and spinal cord. Over the past decade, converging work from neuropathology, imaging and immunology has reframed MS as a B cell–driven disease: CD20⁺ B cells, T cells and myeloid cells interact across the blood–brain barrier, activate microglia and astrocytes through NF-κB–centred cytokine networks, and form meningeal ectopic lymphoid follicles that sustain chronic cortical demyelination and neurodegeneration.

Large longitudinal cohorts now support latent Epstein–Barr virus (EBV) infection in memory B cells as an upstream driver of this cascade, while high-efficacy CD20-depleting antibodies have confirmed the central role of B cells in disease propagation. In parallel, disease-modifying therapies targeting sphingosine 1-phosphate (S1P) receptors, Bruton’s tyrosine kinase (BTK), NF-κB signalling and EBV-directed strategies are reshaping the treatment landscape.

This 2025 review highlights five core mechanistic pillars that dominate current and emerging pipelines—S1P receptor modulation, BTK inhibition, CD20⁺ B-cell depletion, NF-κB–driven glial inflammation and EBV latency—and links each to a practical MS research toolkit, including human UniProt IDs and the full abinScience catalog of recombinant proteins, antibodies, Research Grade biosimilars and ELISA kits.

 Fig 1. The interplay of genetic, environmental, and epigenetic factors in multiple sclerosis risk(2025-10, Vol.10 (1), p.324-40, Article 324)                                               

 Core Target Classes in Multiple Sclerosis 

From a translational perspective, most late-stage MS pipelines can be mapped onto five mechanistic pillars: (1) S1P receptor modulation to control lymphocyte trafficking; (2) BTK inhibition to dampen B-cell and myeloid activation; (3) high-efficacy CD20⁺ B-cell depletion; (4) NF-κB–centred inflammatory cascades in microglia and astrocytes; and (5) therapeutic strategies targeting EBV latency in memory B cells. The table below summarizes representative targets, human genes and UniProt identifiers, together with their core pathological roles.

abinScience Multiple Sclerosis Research Tool kit 

All abinScience products covering MS core pathways are listed below, strictly divided into three categories for easy access.