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GAD-alum treatment induces GAD(65)-specific CD4(+)CD25(high)FOXP3(+) cells in type 1 diabetic patients
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
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2011 (engelsk)Inngår i: CLINICAL IMMUNOLOGY, ISSN 1521-6616, Vol. 138, nr 1, s. 117-126Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

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.

sted, utgiver, år, opplag, sider
Elsevier Science B.V., Amsterdam , 2011. Vol. 138, nr 1, s. 117-126
Emneord [en]
Type 1 diabetes, Immunotherapy, GAD(65), Antigen-specific cell, FOXP3, Cytokine
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Identifikatorer
URN: urn:nbn:se:liu:diva-65953DOI: 10.1016/j.clim.2010.10.004ISI: 000286714000015OAI: oai:DiVA.org:liu-65953DiVA, id: diva2:400667
Tilgjengelig fra: 2011-02-28 Laget: 2011-02-28 Sist oppdatert: 2011-02-28

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