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The Journal of Immunology, 2001, 166: 2831-2841.
Copyright © 2001 by The American Association of Immunologists

Type I Diabetes and Multiple Sclerosis Patients Target Islet Plus Central Nervous System Autoantigens; Nonimmunized Nonobese Diabetic Mice Can Develop Autoimmune Encephalitis1

Shawn Winer2,*, Igor Astsaturov2,*, Roy K. Cheung2,*, Lakshman Gunaratnam*, Violetta Kubiak*, Miguel A. Cortez*, Mario Moscarello*, Paul W. O’Connor{dagger}, Colin McKerlie{ddagger}, Dorothy J. Becker§ and H.-Michael Dosch3,*

* The Hospital For Sick Children, {dagger} St. Michael’s Hospital, University of Toronto, {ddagger} Sunnybrook and Women’s College Health Sciences Center, University of Toronto, Ontario, Canada; and § Children’s Hospital of Pittsburgh, Pittsburgh, PA 15219

Type I diabetes and multiple sclerosis (MS) are distinct autoimmune diseases where T cells target either islet or CNS self-proteins. Unexpectedly, we found that autoreactive T cells in diabetic patients, relatives with high diabetes risk, nonobese diabetic (NOD) mice, and MS patients routinely target classical islet as well as CNS autoantigens. The pathogenic potential of CNS autoreactivity was testable in NOD mice. Pertussis holotoxin, without additional Ags or adjuvants, allowed development of an NOD mouse-specific, autoimmune encephalitis with variable primary-progressive, monophasic, and relapsing-remitting courses. T cells from diabetic donors transferred CNS disease to pertussis toxin-pretreated NOD.scid mice, with accumulation of CD3/IFN-{gamma} transcripts in the brain. Diabetes and MS appear more closely related than previously perceived. NOD mouse-specific, autoimmune encephalitis provides a new MS model to identify factors that determine alternative disease outcomes in hosts with similar autoreactive T cell repertoires.




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