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  • Print publication year: 1996
  • Online publication date: August 2010

8 - Immunopathology and pathophysiology of experimental autoimmune encephalomyelitis

from Part I - Physiology and pathophysiology of nerve fibres

Summary

Introduction

Experimental autoimmune encephalomyelitis (EAE) is an inflammatory demyelinating disease of the central nervous system (CNS), and is widely studied as an animal model of the human CNS demyelinating diseases, including multiple sclerosis (Raine, 1984). EAE can be induced by inoculation with whole CNS tissue, purified myelin basic protein (MBP) or myelin proteolipid protein (PLP), together with adjuvants. It may also be induced by the passive transfer of T cells specifically reactive to these myelin antigens. EAE may have either an acute or a chronic relapsing course. Acute EAE closely resembles the human disease acute disseminated encephalomyelitis, while chronic relapsing EAE resembles multiple sclerosis. EAE is also the prototype for T-cell-mediated autoimmune disease in general. This chapter will focus on the immunopathology and pathophysiology of EAE, which are the subjects of investigation in my laboratory.

Immunopathology

In EAE, activated CD4+ T cells specific for myelin antigens cross the blood–brain barrier and enter the CNS parenchyma. Macrophages, CD4+ T cells of other specificities, and a limited number of B cells and CD8+ T cells also then enter the CNS (Traugott et al., 1981; McCombe et al., 1992). It is generally held that myelin, rather than the oligodendrocyte, is the primary target of the autoimmune attack in EAE (Itoyama & Webster, 1982; Moore, Traugott & Raine, 1984), and that the myelin damage is initiated by macrophages that have been activated by cytokines secreted by the invading T cells.