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Shirai, R.;  Yamauchi, J. Risk Genes and Their Candidates in Multiple Sclerosis. Encyclopedia. Available online: https://encyclopedia.pub/entry/40630 (accessed on 17 July 2025).
Shirai R,  Yamauchi J. Risk Genes and Their Candidates in Multiple Sclerosis. Encyclopedia. Available at: https://encyclopedia.pub/entry/40630. Accessed July 17, 2025.
Shirai, Remina, Junji Yamauchi. "Risk Genes and Their Candidates in Multiple Sclerosis" Encyclopedia, https://encyclopedia.pub/entry/40630 (accessed July 17, 2025).
Shirai, R., & Yamauchi, J. (2023, January 31). Risk Genes and Their Candidates in Multiple Sclerosis. In Encyclopedia. https://encyclopedia.pub/entry/40630
Shirai, Remina and Junji Yamauchi. "Risk Genes and Their Candidates in Multiple Sclerosis." Encyclopedia. Web. 31 January, 2023.
Risk Genes and Their Candidates in Multiple Sclerosis
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This entry is adapted from the peer-reviewed paper 10.3390/neurolint15010003

Oligodendrocytes are central nervous system glial cells that wrap neuronal axons with their differentiated myelin membranes as biological insulators. There has recently been an emerging concept that multiple sclerosis could be triggered and promoted by various risk genes that appear likely to contribute to the degeneration of oligodendrocytes. Despite the known involvement of vitamin D, immunity, and inflammatory cytokines in disease progression, the common causes and key genetic mechanisms remain unknown.

multiple sclerosis oligodendrocyte risk gene

1. Introduction

The myelin sheath is formed as a multilamellar membrane structure through the spiral wrapping of neuronal axons that act as insulators [1][2][3][4]. The transmission of each action potential on a limited membrane region is significantly promoted by the resulting saltatory conduction. Electrical signals are quickly derived to adjacent or distant neuronal cells and neuronal networks. If the myelin is damaged, however, fast signal transmission is not achieved, which causes defective neuronal function. This phenomenon is typically observed in demyelinating states. One well-known demyelinating disease is multiple sclerosis (MS) of the central nervous system (CNS). It is thought that MS is often caused by an abnormal autoimmune reaction in the CNS.
First defined by the National Multiple Sclerosis Society (in the United States) in 1996, MS is a chronic inflammatory disease that is characterized by demyelination mainly in the brain and, in turn, axonal degeneration [5]. The prevalence of MS is higher in Caucasians in the United States and Europe. The incidence rate is more than 100 patients per 100,000 population members in some areas of Northern Europe [6]. In Japan, the prevalence was estimated to be 1 to 5 patients per 100,000 population members, but this number has reportedly increased to 14 to 18 over a single decade [7]. The incidence of MS is increasing in both developed and developing countries [8]. The average age of onset of MS is middle-age and the disease is approximately twice as common in women than in men [9][10].
It is unclear why the number of MS patients has increased recently across countries and regions. There are various risks and possible reasons for the development of the disease, including smoking, vitamin D deficiency, obesity, and Epstein-Barr virus, which is a type of herpes virus [11]. MS also has genetic factors, as first-degree relatives and identical twins have a 25% chance of being affected [12]. The major histocompatibility complex (MHC) HLA-DRB1*15:01 allele was the first factor identified as a risk factor for MS [13]. Subsequent studies have shown that interleukin (IL) 2Rα and IL7R are also genetic factors [14].
MS symptoms likely depend on the tissues and regions where demyelination occurs. Some of the most common symptoms are optic neuritis and brainstem and spinal cord syndromes. Early clinical symptoms usually recover, but relapses are often followed by sequelae [15]. The onset is related to the location and size of the lesion, and even small lesions in the symptomatic zone are likely to cause symptoms, with magnetic resonance imaging showing typical “Dawson’s fingers” with periventricular lesions [16].

2. Gene Risk and Signaling Pathway

Environmental cues associated with the increased risk of developing MS have been established, and over 200 risk loci with moderate to subtle effects have been described. To dissect the influence of genetic predisposition and environmental factors, Florian et al. investigated the peripheral immune signatures of 61 monozygotic twin pairs discordant for MS. They revealed an inflammatory shift in a monocyte cluster of twins with MS, coupled with the emergence of a population of naive helper T cells that have a transient response IL2 as MS-related immune alterations [17]. The research on genetically identical (monozygotic) twins shows that the concordance rate for MS is approximately 30%. This indicates that genetic and environmental factors interact with MS. Baranzini et al. examined DNA methylation and gene expression across the genome in three monozygotic twins discordant for MS; however, there were no consistent differences in DNA sequence [18]. It is surprising that the environment strongly indicated epigenetic modifications to germline susceptibility based on studies of adoptees, half-siblings, and avuncular pairs. The fact that complete explanations for disease heritability were unachieved after whole-genome association studies warrants consideration of all the factors contributing to disease risk, such as genetic, epigenetic, and environmental factors [19].
As many as 200 single-nucleotide polymorphisms (SNPs) are associated with MS risk [20][21][22][23]. Gresle et al. analyzed MS risk expression quantitative trait loci associations for 129 distinct genes in MS patients [24]. They identified the MS risk SNPs, rs2256814 Myelin transcription factor 1 (MYT1) in CD4 cells and rs12087340 RF00136 in monocyte cells. IL7 receptor (IL7R) is a member of the type I cytokine receptor family and is a primary pleiotropic receptor in immune cells. Two GWASs of MS reported that three SNPs outside of the MHC region were associated with MS: rs6897032 within the IL7R gene and two SNPs (rs2104286 and rs12722489) in the IL2R gene [14][25]. Omraninava et al. revealed that the IL7RA gene rs6897932 SNP decreases MS susceptibility [26]. Infection with the herpes virus and Mycoplasma pneumonia create grounds for MS. The T allele in the IFNγ gene (+874) and the genotypes of AA and AG at the TNFα gene (-308) at position−308 were considered potential risk factors for MS [27]. Despite GWASs explaining that there are common SNPs associated with various diseases, known common variants only account for part of the estimated heritability of common complex diseases. Nadia et al. identified the rare functional variants analyzed within a large Italian MS multiplex family with five affected members [28]. Another study showed that up to 5% of MS inheritability may be accounted for by rare variations in the gene coding sequence, with four novel low genes driving MS risk independently of common variant signals [29]. Based on the research of a large cohort of Italian individuals, researchers identified three SNPs (rs4267364, rs8070463, rs67919208) that were involved in the regulation of TBK1 Binding Protein 1 (TBKBP1) and prioritized them as functionally relevant in MS [30]. Recent GWAS research in MS that has analyzed up to 47,000 MS patients and 68,000 healthy controls has determined more than 200 non-MHC genome-wide associations. The results show that immune cells, such as T cells, B cells, and monocytes, have susceptible gene specificity [31]. The International Multiple Sclerosis Consortium analyzed the large-scale GWAS data of 47,000 MS patients and 68,000 healthy controls and established a reference genetic map of MS. Their findings demonstrate the enrichment of MS genes in these brain-resident immune cells, suggesting that they may have a role in targeting an autoimmune process to the CNS, although MS is most likely initially triggered by a perturbation in peripheral immune responses [22].
The Janus kinase and signal transducer and activator of the transcription (JAK/STAT) pathway is essential for both innate and acquired immunity. It has also been reported to be associated with several neuroinflammatory diseases (Figure 1) [32]. In EAE mice, Th1 cells produce interferon-gamma (IFNγ) via STAT4 and inflammatory macrophages, which promote macrophage activation. Similarly, Th17 produces granulocyte-macrophage colony-stimulating factor (GM-CSF) in the CNS and promotes macrophage polarization to inflammation via JAK/STAT5 (Figure 1) [33].
Figure 1. JAK/STAT signaling pathway associated with MS. Cytokines, through JAK/STAT signaling, especially in Th1 and Th17 cells, are putatively considered responsible for the progression of MS.
A comprehensive analysis of genes in the brain of MS patients has shown increased levels of immune cell populations and decreased ones of endothelial cells, Th1 cells, and Treg cells in MS lesions [34]. Toll-like receptors (TLRs) have a variety of roles, including axonal pathway formation and dorsoventral patterning in the CNS. TLR ligands, such as pathogen-associated molecular patterns (PAMPs), have been identified as T cell promoters in MS. In particular, TLR2 expression is high in MS lesions and TLR2 activation induces the expression of pro-inflammatory cytokines such as IL-6, IL-8, and TNF-α, which are implicated in exacerbated inflammation (Figure 2) [35]. The HLA signal in the Italian population maps to a glycoprotein involved in dendritic cell (DC) maturation, such as TNFSF14 gene encoding LIGHT. Miriam et al. reported that the TNFSF14 intronic SNP rs1077667 was the main MS-associated variant in the region. That means that the intronic variant rs1077667 alters the expression of TNFSF14 in DCs, which may play a role in MS pathogenesis [36]. A variant in TNHSH13B, encoding the cytokine and drug target B-cell activating factor (BAFF), was associated with upregulated humoral immunity through increased levels of soluble BAFF, B lymphocytes, and immunoglobulins in MS [37]. Leptin (LEP) and leptin receptor (LEPR) overexpression are related to MS activity and progression, and peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PGC1A) is able to affect the reactive oxygen species production in the pathogenesis of MS. LEP rs7799039 and LEPR rs1137101 genetic variants modify the serum LEP levels and PGC1A rs8192678 alters the PGC1A activity. Ivana et al. revealed that the PGC1A rs8192678 minor allele had an increased risk for the occurrence of MS, and LEP rs7799039 affected the LEP gene expression in relapsing-remitting patients [38].
Figure 2. Interaction of some receptors with their cognate ligands induces the expression of pro-inflammatory cytokines in immune cells. Pathogen-associated molecular patterns interaction with TLRs, SOCS3 activation by cytokine receptors, microbe-associated molecular patterns or damage-associated molecular patterns binding to pattern recognition receptors, and/or activation through NF-κB are involved in the regulation of the expression of inflammatory cytokines, which are responsible for MS, in immune cells.
Furthermore, in relapsing MS, reduced suppression of cytokine signaling-3 (SOCS3) expression in the CNS and immune cells may induce LEP-mediated overexpression of pro-inflammatory cytokines (Figure 2) [39]. Pattern recognition receptors, which are triggered by both microbe-associated molecular patterns and damage-associated molecular patterns, have been reported to regulate innate immune responses in MS and an EAE model. Pattern recognition receptor signaling promotes inflammatory-producing cytokine production in CNS autoimmune diseases (Figure 2) [40]. NF-κB is involved in a wide range of vital processes, including inflammation, cell proliferation, and differentiation. Abnormal NF-κB activation has been reported to be closely associated with the development of MS and EAE [41].
In MS, the altered Foxp3-E2 variant-associated inhibitory activity of Treg cells is associated with defective signaling via IL-2 and glycolysis, which modulates Treg cell induction and function in autoimmunity [42]. The expression of vascular endothelial growth factors and matrix metallopeptidases involved in angiogenesis is increased in MS. These genes are also involved in basement membrane degradation and blood–brain barrier disruption, which allows immune cells to infiltrate the CNS in EAE and MS (Figure 3) [43]. Programmed cell death 1 (PD-1) is known as an immune checkpoint that is associated with several autoimmune diseases. Research on the frequency of PD-1 genotypes and alleles in MS patients shows that PD-1 gene polymorphisms may be associated with MS [44]. Phosphorylation of receptor-interacting protein kinase 1 (RIPK1) in astrocytes and microglia triggers a detrimental neuroinflammatory program that contributes to the neurodegenerative environment in MS (Figure 3) [45].
Figure 3. Abnormal autoimmune reaction and neuroinflammation in MS. Altered Foxp3 expression in Treg cells induces an abnormal autoimmune reaction. Expression levels of vascular endothelial growth factors and matrix metallopeptidases are increased, probably disrupting the blood–brain barrier. This disruption allows immune cells to infiltrate. Phosphorylation of RIPK1 in astrocytes and microglia is involved in the promotion of the neuroinflammatory program.
Risk genes have been well studied by meta-analyses and many SNPs have been identified. MYT1, IL2R, IL7R, IFNγ, and TNFα, among others, are considered to be the major risk genes in MS. The related major signaling in MS is the JAK/STAT pathway.

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