Publication

Multiple sclerosis - a response-to-damage model

't Hart, B. A., Hintzen, R. Q. & Laman, J. D., Jun-2009, In : TRENDS IN MOLECULAR MEDICINE. 15, 6, p. 235-244 10 p.

Research output: Contribution to journalReview articleAcademicpeer-review

According to a widely supported but unproven concept, the autoimmune mechanisms that drive neuroinflammation in multiple sclerosis (MS) are triggered by virus infection. However, a direct viral trigger of MS has not been identified. MS models in non-human primates suggest that lifelong asymptomatic infection with certain herpesviruses (e.g. cytomegalovirus) creates a repertoire of potentially autoreactive memory T cells. When these are exposed to antigens released after central nervous system injury as a consequence of an unknown pathogenic event, they are reactivated and induce autoimmune neurological disease. This response-to-damage of antiviral memory cells can take place years after the initiating infection. Consequently, elucidating the anti-herpesvirus T-cell repertoire might provide new targets for preventive diagnosis and therapy.

Original languageEnglish
Pages (from-to)235-244
Number of pages10
JournalTRENDS IN MOLECULAR MEDICINE
Volume15
Issue number6
Publication statusPublished - Jun-2009
Externally publishedYes

    Keywords

  • EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS, NONHUMAN PRIMATE MODEL, HLA-E, CALLITHRIX-JACCHUS, MOLECULAR MIMICRY, CLONAL EXPANSIONS, COMMON MARMOSETS, CELL RECEPTORS, IN-VITRO, LESIONS

ID: 17763958