Introduction

Experimental allergic (autoimmune) neuritis (EAN) is an autoimmune disease that can be induced by the inoculation of susceptible animals with peripheral nervous system (PNS) antigens and adjuvants. In many respects, EAN is similar to experimental allergic (or autoimmune) encephalomyelitis (EAE). Indeed, studies of EAE paved the way for the development of EAN as a model of inflammatory demyelinating disease of the PNS (Waksman & Adams, 1955). In early studies of EAE, inflammation of the nerve roots was present, but always in combination with inflammation in the central nervous system (CNS) (Innes, 1951; Ferraro & Roizin, 1954). Lumsden (1949) inoculated animals with peripheral nerve, but produced a disease like EAE. Waksman & Adams (1955) deliberately set out to produce an animal model in which inflammation was confined to the PNS and achieved this by inoculating rabbits with peripheral nerve antigens and adjuvants. Acute EAN has subsequently been induced in rats (Smith, Forno & Hofmann, 1979), guinea pigs (Waksman & Adams, 1956; Hall, 1967), mice (Waksman & Adams, 1956; Dieperink et al., 1991), chickens (Petek & Quaglio, 1967) and monkeys (Lumsden, 1949; Wisniewski et al., 1974; Eylar et al., 1982) and serves as a good model of the human disease, the Guillain–Barré syndrome (GBS).