Multiple sclerosis is an autoimmune disease in which the immune system targets the myelin sheaths that surround nerve fibers. The myelin sheaths work like the insulation surrounding an electrical wire, allowing the nerve fibers to transmit information throughout the body. When the immune system attacks the myelin sheath it damages small areas of tissue. These damaged areas are called "lesions". The lesions are effectively gaps over which signals cannot be transmitted, resulting in a wide range of neurological symptoms including loss of sensation and mobility, loss of vision, interference with mental processes, and, in extreme cases, death.

The approaches that TPIMS investigators are taking in their multiple sclerosis research are similar to the approaches used in Type I diabetes research. Specifically, the research focuses on understanding why the immune system attacks and destroys the myelin sheath (Kumar, Sercarz), and designing and testing strategies to re-educate the immune system so that it recognizes the myelin sheath tissue as self (Kumar, Houghten, Pinilla, Sercarz, Wilson).

For many years research in the Davies laboratory has focused on understanding that part of the immune system that actively prevents diseases like type I diabetes and multiple sclerosis in healthy individuals. The idea is that if we understand how the body normally works to prevent these diseases we should be able to replace or enhance these characteristics in patients with disease in order to either, reverse ongoing disease, or, prevent the progress of disease in individuals who are in the early stages of disease, or, inhibit the development of a disease in individuals who have a family history of that disease, and are therefore considered, "at risk." Recently, the Davies group has identified a way of enhancing a characteristic in the body that is linked to protection from type I diabetes. Current work focuses on how this protective characteristic can be controlled.

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