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Original Article
Brief Report
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Volume 345:1036-1040 October 4, 2001 Number 14
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Development of Type 1 Diabetes despite Severe Hereditary B-Cell Deficiency
Stephan Martin, M.D., Dorothea Wolf-Eichbaum, M.D., Gaby Duinkerken, B.Sc., Werner A. Scherbaum, M.D., Hubert Kolb, Ph.D., Jeroen G. Noordzij, M.D., and Bart O. Roep, M.D., Ph.D.

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Type 1 diabetes results from an immune-mediated destruction of pancreatic beta cells. The disease can be transmitted by bone marrow transplantation in humans1 and animals.2,3 Furthermore, T cells that are reactive to several islet autoantigens have been identified in both mice and humans.4,5 Although it is generally accepted that T cells have a role during the disease process, the possible role of B cells and autoantibodies in type 1 diabetes in humans has not been fully resolved. When they are activated, B cells can produce autoantibodies to pancreatic beta-cell antigens — such as glutamic acid decarboxylase 65 (GAD65), insulin, or . . . [Full Text of this Article]

Case Report

Methods

Autoantibody Analyses

T-Cell Proliferation

Flow Cytometry

Cytokine Analyses

DNA Sequencing

Results

Characterization of Immunodeficiency

Characterization of Diabetes

Discussion


Source Information

From the German Diabetes Center, German Diabetes Research Institute, Heinrich Heine University, Düsseldorf, Germany (S.M., W.A.S., H.K.); the Children's Hospital, Hospital Minden, Minden, Germany (D.W.-E.); the Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, the Netherlands (G.D., B.O.R.); and the Department of Immunology, Erasmus University, Rotterdam, the Netherlands (J.G.N.).

Address reprint requests to Dr. Martin at the German Diabetes Center, German Diabetes Research Institute, Heinrich Heine University Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany, or at martin@dfi.uni-duesseldorf.de.

References



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