Just before World War II, Thomas Rivers of the Rockefeller Institute in New York City developed an animal model of MS called experimental allergic encephalomyelitis (EAE), which is now the best studied model of autoimmunity. While very little was understood about MS at this time, scientists knew that people vaccinated against viral illnesses such as rabies were sometimes prone to develop MS-like disease. They assumed this was because the virus within the vaccines was not completely inactivated.

In 1935, Rivers tested this theory by injecting virus-free myelin into laboratory animals. Under the appropriate conditions, he was able to induce the animals he injected to attack their own myelin, proving that nerve tissues, not viruses, were behind the MS-like symptoms. Although this discovery would play a significant role in understanding immunology and how to treat diseases such as MS and was directly related to the development of two approved treatments for MS (Copaxone® and Tysabri®), it was largely ignored at the time.

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