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Defective suppressor function in CD4+CD25+ T-cells from patients with type 1 diabetes

Lindley, S., Dayan, Colin Mark, Bishop, A., Roep, B. O., Peakman, M. and Tree, T. I. M. 2004. Defective suppressor function in CD4+CD25+ T-cells from patients with type 1 diabetes. Diabetes 54 (1) , pp. 92-99. 10.2337/diabetes.54.1.92

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Abstract

Type 1 diabetes is a T-cell–mediated disease that is associated with loss of immunological tolerance to self-antigens. The mechanisms involved in maintenance of peripheral tolerance include a specialized subset of regulatory T-cells (Treg) within the CD4+CD25+ T-cell population, but the function and phenotype of these cells in type 1 diabetes have not been investigated. We hypothesized that a deficiency in the CD4+CD25+ Treg population or its function could contribute to the lack of self-tolerance evident in patients with type 1 diabetes. We show that although levels of CD4+CD25+ T-cells are normal in patients with recent-onset adult type 1 diabetes, the ability of the Tregs in this population to suppress T-cell proliferation during in vitro cocultures is markedly reduced compared with control subjects (P = 0.007). Moreover, in patients with type 1 diabetes, these cocultures display a more proinflammatory phenotype, with increased secretion of interferon-γ (P = 0.005) and decreased interleukin-10 production (P = 0.03). These deficiencies may reflect a disturbance in the balance of the CD4+CD25+ population, because in patients with type 1 diabetes, a higher proportion of these cells coexpress the early activation marker CD69 (P = 0.007) and intracellular CTLA-4 (P = 0.01). These data demonstrate deficiency in function of the CD4+CD25+ Treg population that may influence the pathogenesis of type 1 diabetes.

Item Type: Article
Status: Published
Schools: Medicine
Systems Immunity Research Institute (SIURI)
Subjects: R Medicine > R Medicine (General)
Publisher: American Diabetes Association
ISSN: 0012-1797
Last Modified: 04 Jun 2017 06:41
URI: http://orca.cf.ac.uk/id/eprint/63707

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