Immunology Case Reports

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Editorial - Immunology Case Reports (2025) Volume 8, Issue 2

Autoimmunity and the Nervous System: Mechanisms Behind Multiple Sclerosis

Abdul Reza *

Department of Oncology/Immunology, Zhejiang University, China

*Corresponding Author:
Abdul Reza
Department of Oncology/Immunology,
Zhejiang University,
China
E-mail: rabdul@iums.ac.ir

Received:02-Jan-2025, Manuscript No. AAICR-25-171198; Editor assigned:03-Jan-2025, PreQC No. AAICR-25-171198(PQ); Reviewed:18-Jan-2025, QC No. AAICR-25-171198; Revised:24-Jan-2025, Manuscript No. AAICR-25-171198(R); Published:31-Jan-2025, DOI:10.35841/aaicr-8.2.198

Citation: Reza A. Autoimmunity and the nervous system: Mechanisms behind multiple sclerosis. Immunol Case Rep. 2025;8(2):198

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Introduction

Multiple sclerosis (MS) is a chronic autoimmune disorder that targets the central nervous system (CNS), leading to progressive neurological dysfunction. Characterized by inflammation, demyelination, and neurodegeneration, MS disrupts the communication between the brain, spinal cord, and peripheral organs. The disease affects millions worldwide and remains one of the most enigmatic and debilitating autoimmune conditions. Understanding the mechanisms behind MS is crucial for developing effective treatments and improving patient outcomes. The CNS is composed of neurons and glial cells, with axons wrapped in a protective myelin sheath that facilitates rapid electrical signal transmission. In MS, the immune system mistakenly identifies myelin as a foreign invader and launches an attack. This autoimmune response leads to inflammation, destruction of myelin (demyelination), and eventual axonal damage [1].

The lesions or plaques seen in MRI scans of MS patients are hallmarks of this process. These areas of damage disrupt nerve signaling, resulting in symptoms such as muscle weakness, vision problems, fatigue, and cognitive impairment. At the heart of MS lies a breakdown in immune tolerance. Regulatory T cells (Tregs), which normally suppress immune responses and maintain self-tolerance, become dysfunctional. This failure allows autoreactive T cells—particularly CD4+ T cells—to proliferate and target CNS antigens. Recent research has identified a key molecular player in this dysfunction: PRDM1-S, a primate-specific transcription factor. Overexpression of PRDM1-S leads to increased activity of SGK1, a salt-sensitive kinase that disrupts Treg function and promotes inflammation. Environmental factors such as high dietary salt intake have been shown to exacerbate this pathway, linking lifestyle to disease progression [2].

MS is believed to arise from a complex interplay of genetic predisposition and environmental triggers. Certain HLA alleles, particularly HLA-DRB1*15:01, are strongly associated with increased MS risk. These genetic variants influence antigen presentation and immune activation. Environmental factors also play a significant role. Low vitamin D levels, smoking, Epstein-Barr virus (EBV) infection, and high-fat diets have all been implicated in MS onset and progression. These factors may influence immune regulation, epigenetic modifications, and CNS vulnerability [3].

A critical event in MS pathogenesis is the disruption of the blood-brain barrier (BBB), a selective membrane that protects the CNS from peripheral immune cells. In MS, inflammatory cytokines and matrix metalloproteinases degrade the BBB, allowing autoreactive lymphocytes to infiltrate the CNS. Emerging biomarkers such as neurofilament light chain (NfL) levels in blood and CSF offer insights into axonal  While these therapies can delay progression and reduce relapses, they do not reverse existing damage. Research is ongoing into remyelination strategies and neuroprotective agents. Once inside, these immune cells encounter myelin antigens and initiate a cascade of inflammation. Microglia and astrocytes, the resident immune cells of the CNS, become activated and contribute to tissue damage through the release of pro-inflammatory mediators [4].

The immune attack on myelin leads to its degradation, exposing axons to further damage. Oligodendrocytes, the cells responsible for myelin production, are destroyed or impaired, limiting the CNS’s ability to repair itself. Over time, this results in irreversible axonal loss and neurodegeneration. Neuronal death contributes to the progressive nature of MS, especially in secondary progressive MS (SPMS), where inflammation gives way to chronic neurodegeneration. This phase is less responsive to immunomodulatory therapies and presents a major challenge in treatment [5].

Conclusion

Advances in synthetic biology, gene editing, and personalized medicine hold promise for MS treatment. Therapies targeting PRDM1-S and SGK1 pathways may restore Treg function and halt autoimmunity. Stem cell therapies and regenerative approaches aim to repair damaged myelin and restore neural function. Understanding the molecular mechanisms of MS is key to developing curative therapies. As research continues, the hope is to transform MS from a lifelong burden into a manageable—or even reversible—condition. Symptoms vary widely and may include visual disturbances, motor weakness, sensory deficits, coordination problems, and cognitive decline. The unpredictable nature of MS makes diagnosis and management complex. Diagnosis of MS relies on clinical evaluation, MRI imaging, and cerebrospinal fluid (CSF) analysis. MRI reveals characteristic lesions in the brain and spinal cord, while CSF may show oligoclonal bands—markers of intrathecal antibody production.

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