Neuroimmune Interactions That Operate In The Development And Progression Of Inflammatory Demyelinating Diseases: Lessons From Pathogenesis Of Multiple Sclerosis
Multiple sclerosis (MS) is considered an autoimmune chronic inflammatory disease of the central nervous system (CNS) characterized by demyelination and axonal damage. The view of MS as a “two-stage disease”, with a predominant inflammatory demyelination in the early phase (relapsing-remitting MS form) and a subsequent secondary neurodegeneration in the early phase (secondary or primary progressive MS) of the disease, is now challenged by the demonstration that axonal destruction may occur independently of inflammation and may also produce it. Therefore, as CNS inflammation and degeneration can coexist throughout the course of the disease, MS may be a “simultaneous two-component disease”, in which the combination of neuroinflammation and neurodegeneration promotes irreversible disability. This chapter discusses factors that contribute to the pathogenesis of MS, immune surveillance in the CNS, regulation of immune responses in the inflamed CNS, initiation of T helper 1 (Th1)-mediated immune reactions in the inflamed CNS, amplification of Th1-mediated immune responses in inflamed CNS and tissue damage, and development of autoimmunity in MS.
Oxford Scholarship Online requires a subscription or purchase to access the full text of books within the service. Public users can however freely search the site and view the abstracts and keywords for each book and chapter.
If you think you should have access to this title, please contact your librarian.