| Autor: |
Endl, Josef, Rosinger, Silke, Schwarz, Barbara, Friedrich, Sven-Olaf, Rothe, Gregor, Karges, Wolfram, Schlosser, Michael, Eiermann, Thomas, Schendel, Dolores J., Boehm, Bernhard O. |
| Předmět: |
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| Zdroj: |
Diabetes; Jan2006, Vol. 55 Issue 1, p50-60, 11p, 1 Diagram, 2 Charts, 4 Graphs |
| Abstrakt: |
T-cell-mediated loss of pancreatic β-cells is the crucial event in the development of type 1 diabetes. The phenotypic characteristics of disease-associated T-cells in type 1 diabetes have not yet been defined. The negative results from two intervention trials (the Diabetes Prevention Trial-Type 1 Diabetes and the European Nicotinamide Diabetes Intervention Trial) illustrate the need for technologies to specifcally monitor ongoing autoimmune reactions. We used fluorescence-activated cell sorter analysis to study surface marker expression on T-cell lines specific for two major type 1 diabetes autoantigens, GAD65 and proinsulin. We then applied this knowledge in a cross-sectional approach to delineate the phenotype of circulating memory T-cells. The autoreactive T-cells of patients could be distinguished from those of control subjects by their coexpression of CD25 and CD134. Autoantigen-specific T-cells that recognized multiple GAD65- and preproinsulin-derived peptides and coexpressed CD25+CD134- were confined to patients (n = 32) and pre-diabetic probands (n = 5). Autoantigen-reactive T-cells in control subjects (n = 21) were CD25+CD134- and recognized fewer autoantigen-derived peptides. Insulin therapy did not induce CD25+CD134+ T-cells in type 2 diabetic patients. The coexpression of CD25 and the costimulatory molecule CD134 on memory T-cells provides a novel marker for type 1 diabetes-associated T-cell immunity. The CD134 costimulatory molecule may also provide a novel therapeutic target in type 1 diabetes. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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