Immunopathogenesis of multiple sclerosis

Bernhard Hemmer, Nicole Töpfner, Hans Peter Hartung

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

2 Scopus citations


This chapter provides an overview of immunopathogenesis of multiple sclerosis (MS), which is a chronic disease of the brain and spinal cord. The etiology of MS is unknown, but genes and environmental factors influence the risk of developing the disease. A number of animal models have been developed to study the role of the immune system in central nervous system (CNS) diseases. The most widely used animal model is experimental autoimmune encephalomyelitis (EAE). The changes that occur during the first days of MS lesion development are activation of microglia and macrophages. CD4+ and CD8+ T cells are present in MS lesions. Myelin-specific T cells are central to the autoimmune pathogenesis of EAE. Based on this experimental paradigm, MS has been considered an autoimmune disease mediated by autoreactive T cells. The identification of elevated immunoglobulin G (IgG) antibody levels in the cerebrospinal fluid (CSF) of patients with MS was the first immunological laboratory marker that proved useful in the diagnosis of MS. Several concepts have been discussed to explain the relation between inflammation and neurodegeneration. Axonal damage and loss may be the result of a direct impact of the immune mediators to the neuron or via the loss of protective or nutritive support from glial cells. MS is a chronic disabling disease and its cause remains uncertain, despite considerable progress in research during the past decade. The immune system seems to play a central role in the disease pathogenesis. The involvement of CD8+ T cells and B cells strongly supports the primary inflammatory nature of MS in most patients.

Original languageEnglish
Title of host publicationNeurobiology of Disease
PublisherElsevier Inc.
Number of pages8
ISBN (Print)9780120885923
StatePublished - 2007
Externally publishedYes


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