Autoimmune Neuroinflammation in Central Nervous System Disorders

Autoimmune neuroinflammation encompasses a spectrum of disorders in which aberrant immune responses target components of the central nervous system (CNS), leading to demyelination, neuronal injury and progressive neurological dysfunction. Critical to disease onset and progression is the breach of the blood–brain barrier, allowing autoreactive lymphocytes—particularly T helper 1 and T helper 17 subsets—to infiltrate CNS parenchyma. Within the CNS, resident microglia become activated and release pro-inflammatory cytokines, chemokines and reactive oxygen species, amplifying tissue damage. Oligodendrocyte loss and disrupted myelin integrity underlie conduction deficits, while persistent inflammation drives neurodegeneration. Experimental autoimmune encephalomyelitis remains the principal preclinical model, recapitulating many immunopathological features of human disease and guiding therapeutic innovation. Global efforts seek not only to suppress maladaptive immunity but also to promote remyelination and neurorepair, addressing both acute relapses and chronic progression across multiple sclerosis and related syndromes.

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Autoimmune Neuroinflammation in Central Nervous System Disorders publication trend

The graph below shows the total number of articles in autoimmune neuroinflammation in central nervous system disorders across all publications each year (not limited to Nature Index journals).

Technical terms

Autoimmune neuroinflammation: Immune-mediated attack within the CNS characterised by inflammatory cell recruitment and tissue injury.

Blood–brain barrier (BBB): A specialised endothelial interface that regulates passage of cells and molecules between the circulation and CNS.

Microglia: Resident myeloid cells of the CNS that, when activated, orchestrate inflammatory responses and phagocytic clearance.

Experimental autoimmune encephalomyelitis (EAE): An inducible animal model of CNS autoimmunity used to study disease mechanisms and test therapies.

Neutrophils: Innate immune granulocytes that, upon CNS entry, release enzymes and reactive species capable of exacerbating demyelination and neurodegeneration.

References

1. Clostridium epsilon toxin is excessive in multiple sclerosis and provokes multifocal lesions in mouse models. Journal of Clinical Investigation (2023).
2. Chemogenetic activation of locus coeruleus neurons ameliorates the severity of multiple sclerosis. Journal of Neuroinflammation (2023).
3. Multiple sclerosis: experimental models and reality. Acta Neuropathologica (2016).
4. IKKβ-mediated inflammatory myeloid cell activation exacerbates experimental autoimmune encephalomyelitis by potentiating Th1/Th17 cell activation and compromising blood brain barrier. Molecular Neurodegeneration (2016).
5. Neutrophils: Underestimated Players in the Pathogenesis of Multiple Sclerosis (MS). International Journal of Molecular Sciences (2020).