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From specificity to degeneracy to molecular mimicry: antigen recognition of human autoreactive and pathogen-specific CD4+ T cells

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Advances in the Immunopathogenesis of Multiple Sclerosis
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Abstract

Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS). Although the cause of MS has not been identified, it is widely believed that myelin-specific T cells are somehow involved in the disease process [1]. However it is not clear how these cells become activated and mediate CNS disease. One of the most attractive models for the activation of autoreactive T cells is termed the “molecular mimicry hypothesis” [2]. According to this model, autoreactive T cells become activated in the peripheral immune system by crossreactive ligands derived from infectious agents. After activation and upregulation of adhesion molecules, these cells can cross the blood-brain barrier; after reactivation by myelin antigens either directly or via the recruitment of other cells, the activated T cells damage the myelin sheath and oligodendrocytes.

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© 1999 Springer-Verlag Italia, Milan

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Hemmer, B., Pinilla, C., Gran, B., McFarland, H.F., Houghten, R., Martin, R. (1999). From specificity to degeneracy to molecular mimicry: antigen recognition of human autoreactive and pathogen-specific CD4+ T cells. In: Gambi, D., Muraro, P.A., Lugaresi, A., Ecari, U. (eds) Advances in the Immunopathogenesis of Multiple Sclerosis. Springer, Milano. https://doi.org/10.1007/978-88-470-2269-0_4

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  • DOI: https://doi.org/10.1007/978-88-470-2269-0_4

  • Publisher Name: Springer, Milano

  • Print ISBN: 978-88-470-0067-4

  • Online ISBN: 978-88-470-2269-0

  • eBook Packages: Springer Book Archive

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