Pathophysiology of experimental autoimmune encephalomyelitis

Aleksandar Denic, Bharath Wootla, Istvan Pirko, Ashutosh Mangalam

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Scopus citations

Abstract

Multiple sclerosis (MS) is presumed to be an autoimmune disease of the central nervous system leading to demyelination, axonal damage, and progressive neurologic disability. Although no single animal model can capture all aspects of human MS, the experimental autoimmune encephalomyelitis (EAE) model in rodents immensely improved our understanding of MS pathophysiology. The main advantage of EAE is the genetic engineering of mice to allow researchers to investigate the roles of various genes/molecules in the disease. Data generated from EAE models suggest that disease onset results from an aberrant, T cell-mediated immune response to a number of myelin antigens. We also discuss the importance of other immune cells, such as CD8+ T cells, B cells, and macrophages, in the immunopathogenesis of the disease. In summary, the EAE model has helped to elucidate the roles of various cells/molecules in the neuro-inflammatory aspects of MS.

Original languageEnglish (US)
Title of host publicationMultiple Sclerosis
Subtitle of host publicationA Mechanistic View
PublisherElsevier Inc.
Pages249-280
Number of pages32
ISBN (Electronic)9780128010051
ISBN (Print)9780128007631
DOIs
StatePublished - Jan 1 2015

Keywords

  • B cells
  • CD4 T cells
  • CD8 T cells
  • Experimental autoimmune encephalomyelitis
  • Macrophages
  • Multiple sclerosis
  • Regulatory T cells
  • Th1/Th17 response

ASJC Scopus subject areas

  • Medicine(all)

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    Denic, A., Wootla, B., Pirko, I., & Mangalam, A. (2015). Pathophysiology of experimental autoimmune encephalomyelitis. In Multiple Sclerosis: A Mechanistic View (pp. 249-280). Elsevier Inc.. https://doi.org/10.1016/B978-0-12-800763-1.00011-7