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.

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. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

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. Abstract Text:

Keiko Fukushima,Norio Abiru,Yuji Nagayama,Masakazu Kobayashi,Tsuyoshi Satoh,Mami Nakahara,Eiji Kawasaki,Hironori Yamasaki,Satoshi Ueha,Koji Matsushima,Edwin Liu,Katsumi Eguchi,

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.

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. Publishing Authors By Initials

K Fukushima,N Abiru,Y Nagayama,M Kobayashi,T Satoh,M Nakahara,E Kawasaki,H Yamasaki,S Ueha,K Matsushima,E Liu,K Eguchi,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

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. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Biochemical and biophysical research communication

VOLUME: 367

Page Numbers: 719-24

Journal Abbreviation: Biochem. Biophys. Res. Commun.

ISSN: 1090-2104

DAY: 14

MONTH: 01

YEAR: 2008

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. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 372516

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. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: 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. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for 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.

AFFILIATION: Department of Endocrinology and Metabolism, Unit of Translational Medicine, Graduate School of Biomedical Science, Nagasaki University, Nagasaki, Japan.

Country: United States

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Biochem Biophys Res Commun

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

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 Related Publications

• A multicenter study of leukocytapheresis in rheumatoid arthritis.
• Abrogation of constitutive STAT3 activity sensitizes human hepatoma cells to TRAIL-mediated apoptosis.
• Activation of endothelial nitric oxide synthase by the angiotensin II type 1 receptor.
• Adaptive control of the ethanol-forming system in heterolactic acid bacteria. Effect of growth conditions on alcohol dehydrogenase synthesis in Leuconostoc mesenteroides.
• Adiponectin versus angiotensin II: Key pathological role of their misbalance.
• Angiotensin II signal transduction through the AT1 receptor: novel insights into mechanisms and pathophysiology.
• Biosynthesis of archaeal membrane lipids: digeranylgeranylglycerophospholipid reductase of the thermoacidophilic archaeon Thermoplasma acidophilum.
• Bone edema determined by magnetic resonance imaging reflects severe disease status in patients with early-stage rheumatoid arthritis.
• Cerebellar ataxia in a patient receiving calcineurin inhibitors after living donor liver transplantation: a case report.
• Clearance of hepatitis C virus after living-donor liver transplantation in spite of residual viremia on end date of interferon therapy before transplantation.
• EGF activates PI3K-Akt and NF-kappaB via distinct pathways in salivary epithelial cells in Sjögren's syndrome.
• Easier understanding of pleural indentation on computed tomography.
• Effect of Cibacron Blue F3GA on phosphoglycerate kinase of Lactobacillus plantarum and phosphoglycerate mutase of Leuconostoc dextranicum.
• Epidermal growth factor inhibits Fas-mediated apoptosis in salivary epithelial cells of patients with primary Sjögren's syndrome.
• Exchange reactions catalyzed by methioninase from Pseudomonas putida.
• Exchange reactions catalyzed by methioninase from Pseudomonas putida. Isolation and characterization of the exchange products.
• Functional analysis of type 1 isopentenyl diphosphate isomerase from Halobacterium sp. NRC-1.
• Increasing hepatitis C virus-associated hepatocellular carcinoma mortality and aging: Long term trends in Japan.
• Irreversible imatinib-induced pneumonitis following long-term imatinib administration.
• La autoantigen translocates to cytoplasm after cleavage during granzyme B-mediated cytotoxicity.
• Mechanism of endothelial nitric oxide synthase phosphorylation and activation by thrombin.
• Progress in pathogenesis and therapy of vasculitis syndrome.
• Purification and characterization of methioninase from Pseudomonas putida.
• Recent advancement of understanding pathogenesis of type 1 diabetes and potential relevance to diabetic nephropathy.
• Small GTP-binding proteins and mitogen-activated protein kinases as promising therapeutic targets of vascular remodeling.
• Structure of 2-deoxy-scyllo-inosose synthase, a key enzyme in the biosynthesis of 2-deoxystreptamine-containing aminoglycoside antibiotics, in complex with a mechanism-based inhibitor and NAD+.
• Systematic search for single nucleotide polymorphisms in a lymphoid tyrosine phosphatase gene (PTPN22): Association between a promoter polymorphism and type 1 diabetes in Asian populations. American Journal of Medical Genetics 140A:586-593 (2006).
• Systematic search for single nucleotide polymorphisms in a lymphoid tyrosine phosphatase gene (PTPN22): association between a promoter polymorphism and type 1 diabetes in Asian populations.
• Use of an otolith-deficient mutant in studies of fish behavior in microgravity.
• [Analysis of a mutant Medaka fish ha--ground and parabolic experiments]