GAD-alum treatment induces GAD(65)-specific CD4(+)CD25(high)FOXP3(+) cells in type 1 diabetic patients
2011 (English)In: CLINICAL IMMUNOLOGY, ISSN 1521-6616, Vol. 138, no 1, 117-126 p.Article in journal (Refereed) Published
Type 1 diabetes results from autoimmune destruction of insulin producing pancreatic beta-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(+)CD25(high) 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. GAD(65)-stimulation enhanced the percentage of CD4(+)CD25(high)FOXP3(+) cells, but reduced the percentage of CD4(+)CD25(+) cells, in samples from the GAD-alum treated group. Further, the GAD(65)-induced secretion of IL-5, -10, and -13 correlated with the expression of CD4(+)CD25(high)FOXP3(+) cells, but inversely with CD4(+)CD25(+) cells. These new data suggest that GAD-alum treatment induced GAD(65)-specific T cells with regulatory features.
Place, publisher, year, edition, pages
Elsevier Science B.V., Amsterdam , 2011. Vol. 138, no 1, 117-126 p.
Type 1 diabetes, Immunotherapy, GAD(65), Antigen-specific cell, FOXP3, Cytokine
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-65953DOI: 10.1016/j.clim.2010.10.004ISI: 000286714000015OAI: oai:DiVA.org:liu-65953DiVA: diva2:400667