期刊
DIABETES
卷 54, 期 5, 页码 1407-1414出版社
AMER DIABETES ASSOC
DOI: 10.2337/diabetes.54.5.1407
关键词
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资金
- NIAID NIH HHS [AI39250, AI42288] Funding Source: Medline
CD4(+)CD25(+) T-cells appear to play a crucial role in regulating the immune response. Therefore, we evaluated the peripheral blood frequency and function of CD4(+) CD25(+) T-cells in 70 type 1 diabetic patients and 37 healthy individuals. Interestingly, a positive correlation was observed between increasing age and CD4(+)CD25(+) T-cell frequency in both subject groups. In contrast to previous studies of nonobese diabetic mice and type 1 diabetic patients, similar frequencies of CD4(+)CD25(+) and CD4(+)CD25(+Bright) T-cells were observed in healthy control subjects and type 1 diabetic patients of similar age. There was no difference between type 1 diabetic subjects of recent-onset versus those with established disease in terms of their CD4(+)CD25(+) or CD4(+)CD25(+Bright) T-cell frequency. However, type 1 diabetic patients were markedly defective in their ability to suppress the proliferation of autologous effector T-cells in vitro. This type 1 diabetes-associated defect in suppression was associated with reduced production of interleukin (IL)-2, gamma-interferon, and transforming growth factor-beta, whereas other cytokines including those of adaptive and innate immunity (IL-10, IL-1 beta, IL-6, IL-8, IL-12p70, and tumor necrosis factor-a) were similar in control subjects and type 1 diabetic patients. These data suggest that age strongly influences the frequency of CD4(+)CD25(+) T-cells and that function, rather than frequency, may represent the means by which these cells associate with type 1 diabetes in humans.
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