IDDM (type I diabetes) is generally believed to result from T-cell-mediated autoimmune destruction of the insulin-producing β-cells in the pancreatic islets of Langerhans. In the last few years, considerable progress has been made with regard to the identification and characterization of candidate autoantigens recognized by autoantibodies; several of these candidate autoantigens are recognized by T-cells, including insulin, GAD65 and GAD67, heat-shock protein 65 (hsp65), and islet-cell antigen 69 (ICA69). In addition to these, a number of unidentified β-cell antigens, including insulin-secretory granule membrane proteins and a 38-kDa protein, have been shown to stimulate T-cells of IDDM patients. However, T-cell autoreactivity to islet antigens is not specific for IDDM, and the T-cell target antigens are not specific for β-cells. Moreover, the autoantigens involved in the initiation of the insulitis must be defined, and the mechanism of the T-cell-dependent β-cell destruction remains to be unraveled. This review focuses on T-cell autoreactivity in IDDM in humans and the implications of the present knowledge for immunointervention and monitoring of immunotherapeutic trials.
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Perspectives in Diabetes|
September 01 1996
T-Cell Responses to Autoantigens in IDDM: The Search for the Holy Grail
Bart O Roep
Bart O Roep
Department of Imnumohaematology and Blood Bank, University Hospital Leiden
Leiden, The Netherlands
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Address correspondence and reprint requests to Dr. Bart 0. Roep, Dept. Immunohaematology & Blood Bank, University Hospital, P.O. Box 9600, NL-2300 RC Leiden, The Netherlands.[email protected].
Diabetes 1996;45(9):1147–1156
Article history
Received:
February 05 1996
Revision Received:
May 06 1996
Accepted:
May 06 1996
PubMed:
8772714
Citation
Bart O Roep; T-Cell Responses to Autoantigens in IDDM: The Search for the Holy Grail. Diabetes 1 September 1996; 45 (9): 1147–1156. https://doi.org/10.2337/diab.45.9.1147
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