Autoimmunity and beta Cell Regeneration in Mouse and Human Type 1 Diabetes: The Peace Is Not Enough

doi:10.1196/annals.1394.006

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How Do We Best Employ Animal Models for Type 1 Diabetes and Multiple Sclerosis? Volume 1103 published April 2007
Ann. N.Y. Acad. Sci. 1103: 19–32 (2007). doi: 10.1196/annals.1394.006
Copyright © 2007 by the New York Academy of Sciences
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Part I. Controversies Surrounding the Use of Animal Models in Type 1 Diabetes and Multiple Sclerosis
Autoimmunity and $beta$ Cell Regeneration in Mouse and Human Type 1 Diabetes

The Peace Is Not Enough

VITALY ABLAMUNITS^a, NICOLE A. SHERRY^b, JAKE A. KUSHNER^c AND KEVAN C. HEROLD^a

^{^a} Section of Immunobiology and Department of Medicine, Yale University, New Haven, Connecticut, USA ^{^b} Department of Pediatrics, Massachusetts General Hospital, Boston, Massachusetts, USA ^{^c} Division of Endocrinology, Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA

Key Words: immune therapy • type 1 diabetes • $beta$ cell regeneration

Address for correspondence: Kevan C. Herold, M.D., Yale University School of Medicine, 300 Cedar St., S155-B, New Haven, CT 06520. Voice: 203-785-6507; fax: 203-785-3674. kevan.herold{at}yale.edu

Accumulating data from animal models of type 1 diabetes andsome findings from clinical studies suggest that autoimmunedestruction of islet $beta$ cells is associated with enhanced $beta$ cellregeneration. Successful immune therapies, aimed at preservationof islet cell mass, result in a remarkable reduction of $beta$ cellregeneration. Treated or not, as long as the task of treatmentis limited by "making peace" with autoimmunity, the processof $beta$ cell loss continues. Additional therapeutic modalities capableof stimulating $beta$ cell regeneration in the absence of active autoimmunedestruction are urgently needed.