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Novartis Found Symp. 2008;292:159-71; discussion 171-3, 202-3.

Immune markers of disease and therapeutic intervention in type 1 diabetes.

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Department of Immunohaematology and Blood Transfusion, E3-Q, Leiden University Medical Center, PO Box 9600, NL-2300 RC Leiden, The Netherlands.


Type 1 diabetes results from a T cell-mediated autoimmune destruction of the insulin-producing pancreatic beta cells in subjects with a genetic predisposition to this disease. Therapies directed against T cells have been shown to halt the disease process and prevent recurrent beta cell destruction after islet transplantation. Less is known about the mechanisms by which T cell-targeted therapies modify disease, how the immune system may suppress autoreactivity, and whether (or which) autoantigen(s) are critically involved in disease modulation. Autoreactive T cells have proven to be valuable tools to study pathogenic or diabetes-related processes. Measuring T cell autoreactivity has also provided critical information to determine the fate of islet allografts transplanted to type 1 diabetic patients. Unfortunately, cellular autoimmunity is a difficult study subject, and most activities were aiming at defining disease-associated T cell responses. A perhaps even more important goal will be to define and measure changes in T cell autoimmunity that are associated with disease intervention following immunotherapy, as autoantibodies do not qualify for this purpose. Recently, we have identified immune markers that associate with remission after initiation of insulin therapy ('honeymoon'), and disease suppression with antibody therapy (ATG, daclizumab, anti-CD3) or islet autoantigen. The challenge for the future is to determine which immune factors associate with tolerance to beta cell antigens, and to define what measures T cells can provide to suppress autoreactivity.

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