The role of T cells and the innate immune system in the pathogenesis of theiler's virus demyeliating disease

Julie K. Olson, Stephen D. Miller

Research output: Chapter in Book/Report/Conference proceedingChapter

6 Scopus citations

Abstract

The immune response to TMEV involves activation of both the innate and adaptive immune responses. The innate immune response is the initial response by the host to a viral infection. The adaptive immune response follows the initial response and is mediated by CD8+ and CD4+ T cell and antibody responses specific to the viral antigens. CNS pathogenesis in TMEV-IDD is associated with long-term virus persistence in CNS-resident microglia and macrophages which leads to the activation of a virus-specific CD4+ Th1 response. Myelin destruction is initiated by the bystander effector functions of CNS-resident mononuclear cells which are activated both directly by the innate immune response to persistent TMEV infection and indirectly by pro-inflammatory cytokines released by virus-specific Th1 cells. Initial myelin destruction leads to the release of myelin antigens and the subsequent activation of myelin epitope-specific autoreactive CD4+ Th1 cells via epitope spreading which are largely responsible for chronic disease progression.

Original languageEnglish (US)
Title of host publicationExperimental Models of Multiple Sclerosis
PublisherSpringer US
Pages645-657
Number of pages13
ISBN (Electronic)9780387255187
ISBN (Print)0387255176, 9780387255170
DOIs
StatePublished - Jan 1 2005

Keywords

  • Theiler's murine encephalomyelitis virus (TMEV)
  • demyelinating disease
  • epitope spreading
  • molecular mimicry
  • multiple sclerosis

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