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T Cells of Multiple Sclerosis Patients Target a Common Environmental Peptide that Causes Encephalitis in Mice¹

Shawn Winer^2,*, Igor Astsaturov^2,*, Roy K. Cheung^2,*, Katrin Schrade^*, Lakshman Gunaratnam^*, Denise D. Wood^*, Mario A. Moscarello^*,¶, Paul O’Connor, Colin McKerlie, Dorothy J. Becker and Hans-Michael Dosch^3,*,

^* The Hospital For Sick Children, Research Institute, Division of Neurology, St. Michael’s Hospital, and Division of Laboratory Animal Services, Sunnybrook Hospital, and Departments of Paediatrics and ^¶ Medicine, University of Toronto, Toronto, Ontario, Canada; and ^|| Department of Pediatrics, Division of Endocrinology, Children’s Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA 15260

Multiple sclerosis (MS) is a chronic autoimmune disease triggered by unknown environmental factors in genetically susceptible hosts. MS risk was linked to high rates of cow milk protein (CMP) consumption, reminiscent of a similar association in autoimmune diabetes. A recent rodent study showed that immune responses to the CMP, butyrophilin, can lead to encephalitis through antigenic mimicry with myelin oligodendrocyte glycoprotein. In this study, we show abnormal T cell immunity to several other CMPs in MS patients comparable to that in diabetics. Limited epitope mapping with the milk protein BSA identified one specific epitope, BSA₁₉₃, which was targeted by most MS but not diabetes patients. BSA₁₉₃ was encephalitogenic in SJL/J mice subjected to a standard protocol for the induction of experimental autoimmune encephalitis. These data extend the possible, immunological basis for the association of MS risk, CMP, and CNS autoimmunity. To pinpoint the same peptide, BSA₁₉₃, in encephalitis-prone humans and rodents may imply a common endogenous ligand, targeted through antigenic mimicry.

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