Plasma concentrations of soluble IL-2 receptor α (CD25) are increased in type 1 diabetes and associated with reduced C-peptide levels ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-02

AUTHORS

Kate Downes, M. Loredana Marcovecchio, Pamela Clarke, Jason D. Cooper, Ricardo C. Ferreira, Joanna M. M. Howson, Jennifer Jolley, Sarah Nutland, Helen E. Stevens, Neil M. Walker, Chris Wallace, David B. Dunger, John A. Todd

ABSTRACT

AIMS/HYPOTHESIS: Type 1 diabetes is a common autoimmune disease that has genetic and environmental determinants. Variations within the IL2 and IL2RA (also known as CD25) gene regions are associated with disease risk, and variation in expression or function of these proteins is likely to be causal. We aimed to investigate if circulating concentrations of the soluble form of CD25, sCD25, an established marker of immune activation and inflammation, were increased in individuals with type 1 diabetes and if this was associated with the concentration of C-peptide, a measure of insulin production that reflects the degree of autoimmune destruction of the insulin-producing beta cells. METHODS: We used immunoassays to measure sCD25 and C-peptide in peripheral blood plasma from patient and control samples. RESULTS: We identified that sCD25 was increased in patients with type 1 diabetes compared with controls and replicated this result in an independent set of 86 adult patient and 80 age-matched control samples (p = 1.17 × 10(-3)). In 230 patients under 20 years of age, with median duration-of-disease of 6.1 years, concentrations of sCD25 were negatively associated with C-peptide concentrations (p = 4.8 × 10(-3)). CONCLUSIONS/INTERPRETATION: The 25% increase in sCD25 in patients, alongside the inverse association between sCD25 and C-peptide, probably reflect the adverse effects of an on-going, actively autoimmune and inflammatory immune system on beta cell function in patients. More... »

PAGES

366-372

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00125-013-3113-8

    DOI

    http://dx.doi.org/10.1007/s00125-013-3113-8

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1052333643

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/24264051


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