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Editorial

A Tale of Two Cousins: Type 1 and Type 2 Diabetes

¹ Institut National de la Santé et de la Recherche Médicale U561, St. Vincent de Paul Hospital, Paris, France
² Department of Molecular Medicine, Division of Endocrinology & Diabetes, Karolinska Hospital, Stockholm, Sweden
³ Metabolism Unit, CNR Institute of Clinical Physiology, University of Pisa, Pisa, Italy
⁴ Unit of Endocrinology and Metabolism, University of Louvain, Brussels, Belgium
⁵ Howard Hughes Medical Institute, University of Chicago, Chicago, Illinois
⁶ Department of Endocrinology and Metabolism, Hebrew University Hadassah Medical Center, Jerusalem, Israel

Address correspondence and reprint requests to Christian Boitard, Unité INSERM U.561, Hôpital Saint Vincent de Paul, 82 Avenue Denfert-Rochereau, 75014, Paris, France. E-mail: christian.boitard@paris5.inserm.fr

Key Words: IA-2, insulinoma-associated protein 2 • LADA, latent autoimmune diabetes in adults • TNF, tumor necrosis factor • VNTR, variable number of tandem repeats

The first 300 words of the full text of this article appear below.

Insulin secretion and ß-cell biology are the main theme of the Servier-IGIS Meetings that have been held yearly since 2000 in St. Jean Cap Ferrat in southern France (1–5). Previous symposia have mostly focused on insulin secretion and its relationship with ß-cell defects in type 2 diabetes. Type 1 diabetes has not previously been considered, since it is generally viewed exclusively as an autoimmune disease. However, the pathophysiology of either disease is centered on ß-cells, and type 1 and type 2 diabetes share many concerns, especially the goal of preserving or restoring a normal functional ß-cell mass.

Evidence has accumulated that immune tolerance reflects a permanent cross talk between the different cells involved in immune survey functions and peripheral tissues, as in the case of ß-cells in type 1 diabetes. As in most common autoimmune diseases, the problem of the antigenic specificity of the autoimmune reaction that drives the ß-cell damage has been one with most unpredictable issues over the past 20 years. Whether the activation of autoimmunity proceeds from intrinsic immune dysregulation or requires the presence of ß-cells is now no longer a question. Against all predictions, the search for the "diabetes autoantigen" has resulted in a long list of candidates with rather loose identification criteria. All presently high-ranking ß-cell autoantigens are defined as proteins expressed by ß-cells, not as ß-cell–specific antigens. Indeed, evidence has accumulated to indicate that B- and T-cells recognize many autoantigens, rather than a single autoantigen, during diabetes development and that most autoantigens are not ß-cell specific. This makes type 1 diabetes a ß-cell disease rather than an antigen-specific immune disease.

As for type 2 diabetes, there is overwhelming evidence that it cannot be considered exclusively from the angle of the ß-cell. ß-Cells are at the center of multiple physiological loops . . . [Full Text of this Article]

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