To the Editor.
—Acute demyelinating optic neuritis is an important feature of both experimental allergic encephalomyelitis (EAE) and multiple sclerosis. Elucidation of the immunologic mechanisms involved in EAE should expose the processes responsible for causing experimental allergic optic neuritis (EAON). Understanding the causes of EAON should, in turn, shed light on the immunologic events associated with naturally occurring forms of optical neuritis.It is commonly thought that EAE is simply the result of an autoimmune response directed specifically at myelin basic protein (MBP) within myelin.1 Several well-established observations, however, cast doubt on this widespread notion. In the first place, while cellular immunity to MBP or its active peptides is no doubt necessary for EAE induction, it is clearly not sufficient to elicit the disease. High levels of lymphocytes activated against MBP have been found in many experimental and clinical situations in the absence of clinical EAE.2 Furthermore, while
Root-Bernstein R, Westall FC. Optic Neuritis: Mechanism of Induction by Dual Antigen Complex. Arch Ophthalmol. 1983;101(3):486. doi:10.1001/archopht.1983.01040010486038
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