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GAD-alum treatment induces GAD65-specific CD4+CD25highFOXP3+ cells in type 1 diabetic patients.
Jönköping University, School of Health Science, HHJ. Biomedical Platform. Jönköping University, School of Health Science, HHJ, Dep. of Natural Science and Biomedicine.
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2011 (English)In: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 138, no 1, 117-126 p.Article in journal (Refereed) Published
Abstract [en]

Type 1 diabetes results from autoimmune destruction of insulin producing pancreatic β-cells. We have shown that treatment with alum-formulated glutamic acid decarboxylase 65 (GAD-alum) preserved residual insulin secretion and induced antigen-specific responses in children with recent onset type 1 diabetes. The aim of this study was to further investigate the immunomodulatory effect of GAD-alum, focusing on CD4+CD25high cells and their association to cytokine secretion. Samples obtained 21 and 30 months after the initial injection of GAD-alum or placebo were included in the present study. GAD65-stimulation enhanced the percentage of CD4+CD25highFOXP3+ cells, but reduced the percentage of CD4+CD25+ cells, in samples from the GAD-alum treated group. Further, the GAD65-induced secretion of IL-5, -10, and -13 correlated with the expression of CD4+CD25highFOXP3+ cells, but inversely with CD4+CD25+ cells. These new data suggest that GAD-alum treatment induced GAD65-specific T cells with regulatory features.

Place, publisher, year, edition, pages
2011. Vol. 138, no 1, 117-126 p.
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Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:hj:diva-14749DOI: 10.1016/j.clim.2010.10.004PubMedID: 21044870OAI: oai:DiVA.org:hj-14749DiVA: diva2:402119
Available from: 2011-03-07 Created: 2011-03-07 Last updated: 2012-01-16Bibliographically approved

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