Jump to ContentJump to Main Navigation
Neurovascular MedicinePursuing Cellular Longevity for Healthy Aging$
Users without a subscription are not able to see the full content.

Kenneth Maiese

Print publication date: 2009

Print ISBN-13: 9780195326697

Published to Oxford Scholarship Online: January 2010

DOI: 10.1093/acprof:oso/9780195326697.001.0001

Show Summary Details
Page of

PRINTED FROM OXFORD SCHOLARSHIP ONLINE (oxford.universitypressscholarship.com). (c) Copyright Oxford University Press, 2020. All Rights Reserved. An individual user may print out a PDF of a single chapter of a monograph in OSO for personal use. date: 01 December 2020

Neuroimmune Interactions That Operate In The Development And Progression Of Inflammatory Demyelinating Diseases: Lessons From Pathogenesis Of Multiple Sclerosis

Neuroimmune Interactions That Operate In The Development And Progression Of Inflammatory Demyelinating Diseases: Lessons From Pathogenesis Of Multiple Sclerosis

Chapter:
(p.291) Chapter 12 Neuroimmune Interactions That Operate In The Development And Progression Of Inflammatory Demyelinating Diseases: Lessons From Pathogenesis Of Multiple Sclerosis
Source:
Neurovascular Medicine
Author(s):

Enrico Fainardi

Massimiliano Castellazzi

Publisher:
Oxford University Press
DOI:10.1093/acprof:oso/9780195326697.003.0012

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.

Keywords:   central nervous system, immune surveillance, neuroinflammation, tissue damage, multiple sclerosis, pathogenesis, immune responses, neurodegeneration, autoimmunity

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.

Please, subscribe or login to access full text content.

If you think you should have access to this title, please contact your librarian.

To troubleshoot, please check our FAQs , and if you can't find the answer there, please contact us .