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Combined insulin B:9-23 self-peptide and polyinosinic-polycytidylic acid accelerate insulitis but inhibit development of diabetes by increasing the proportion of CD4+Foxp3+ regulatory T cells in the islets in non-obese diabetic mice.


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Title: Combined insulin B:9-23 self-peptide and polyinosinic-polycytidylic acid accelerate insulitis but inhibit development of diabetes by increasing the proportion of CD4+Foxp3+ regulatory T cells in the islets in non-obese diabetic mice.
Authors: Fukushima, Keiko / Abiru, Norio / Nagayama, Yuji / Kobayashi, Masakazu / Satoh, Tsuyoshi / Nakahara, Mami / Kawasaki, Eiji / Yamasaki, Hironori / Ueha, Satoshi / Matsushima, Koji / Liu, Edwin / Eguchi, Katsumi
Issue Date: 21-Mar-2008
Publisher: Elsevier Inc.
Citation: Biochemical and biophysical research communications, 367(4), pp.719-724; 2008
Abstract: Insulin peptide B:9-23 is a major autoantigen in type 1 diabetes. Combined treatment with B:9-23 peptide and polyinosinic-polycytidylic acid (poly I:C), but neither alone, induce insulitis in normal BALB/c mice. In contrast, the combined treatment accelerated insulitis, but prevented diabetes in NOD mice. Our immunofluorescence study with anti-CD4/anti-Foxp3 revealed that the proportion of Foxp3 positive CD4(+)CD25(+) regulatory T cells (Tregs) was elevated in the islets of NOD mice treated with B:9-23 peptide and poly I:C, as compared to non-treated mice. Depletion of Tregs by anti-CD25 antibody hastened spontaneous development of diabetes in non-treated NOD mice, and abolished the protective effect of the combined treatment and conversely accelerated the onset of diabetes in the treated mice. These results indicate that poly I:C combined with B:9-23 peptide promotes infiltration of both pathogenic T cells and predominantly Tregs into the islets, thereby inhibiting progression from insulitis to overt diabetes in NOD mice.
Keywords: CD4+ T cell / Insulin / Insulitis / Non-obese diabetic mouse / Peptide / Polyinosinic-polycytidylic acid / Regulatory T cell / Type 1 diabetes
URI: http://hdl.handle.net/10069/22768
ISSN: 0006291X
DOI: 10.1016/j.bbrc.2007.12.191
PubMed ID: 18194666
Rights: Copyright © 2008 Elsevier Inc. All rights reserved.
Type: Journal Article
Text Version: author
Appears in Collections:Articles in academic journal

Citable URI : http://hdl.handle.net/10069/22768

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