| Autor: |
Karges, Beate, Durinovic-Belló, Ivana, Heinze, Eberhard, Debatin, Klaus-Michael, Boehm, Bernhard, Karges, Wolfram |
| Zdroj: |
Diabetes/Metabolism Research & Reviews; May2006, Vol. 22 Issue 3, p184-189, 6p |
| Abstrakt: |
Background Preservation of beta cell function is a central goal in type 1 diabetes (type 1 DM) immune intervention. The characterization of individuals with recovery from established type 1 DM should provide insight into regulatory mechanisms of beta cell autoimmunity. Methods We studied a patient with antibody-positive type 1 DM with complete recovery of beta cell function for an observation period of 60 months. Using a preproinsulin (PPI) peptide library approach and in vitro cytokine profiling, cellular autoimmunity was characterized in peripheral blood mononuclear cells (PBMC) and CD4+ T-helper cell subsets. Results A predominant secretion of interleukin-10 (IL-10) was detected in the patient's PBMC, mostly attributable to naïve and recently primed CD45+RA+ T cells, with limited PPI epitope recognition. In contrast to a cohort of patients with permanent type 1 DM, interferon-γ secretion was low in PBMC and CD45+RA+, but not in CD45+RA− insulin-reactive T lymphocytes. Autoantibodies against islet cells, tyrosine phosphatase IA-2, GAD65 and insulin were positive at diabetes onset, but gradually declined during follow-up. Conclusions Our observations support the concept that IL-10-dependent regulatory CD4+ T-cell pathways are involved in beta cell recovery after the onset of hyperglycemia in autoimmune type 1 DM. Copyright © 2005 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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