Two questions were posed at the beginning of this article. Is EAE a good model 
for MS? And, is MS an autoimmune disease? The first question is easier to 
address than the second. EAE is the best available model for the inflammatory 
processes that occur in MS, and for the disease process. The latter depends 
somewhat on study of chronic relapsing EAE, rather than early or mono-episodic 
EAE, which, although of great immunological interest, is of less relevance to 
the established disease that presents as MS. The second question asks whether MS 
fulfills Koch's postulates as an autoimmune disease. MS has all the hallmarks of 
an inflammatory disease of the CNS. The question then is whether the 
inflammation is autoimmune. The evidence presented shows a considerable 
autoimmune component to MS inflammation, raising the subsidiary question of 
whether autoimmune reactivity induces MS. This remains unanswerable for the 
present, and it should be kept in mind that the same question also would be 
unanswerable by observation of EAE. The major postulate therefore remains 
unfulfilled. Diagnosis of MS as an autoimmune disease requires definitive 
identification of the autoantigen; otherwise, the possibility remains open that 
this is a disease resulting from the inadvertent activation and dysregulation of 
immune processes in the CNS that, themselves, are not directed at that organ.