ID 109647
Author
Moritani, Maki Otsuka Department of Clinical and Molecular Nutrition, School of Medicine, The University of Tokushima
Yoshimoto, Katsuhiko Otsuka Department of Clinical and Molecular Nutrition, School of Medicine, The University of Tokushima Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Wong, Susan F. Section of Immunobiology, Yale University School of Medicine
Tanaka, Chisato Otsuka Department of Clinical and Molecular Nutrition, School of Medicine, The University of Tokushima KAKEN Search Researchers
Yamaoka, Takashi Otsuka Department of Clinical and Molecular Nutrition, School of Medicine, The University of Tokushima
Sano, Toshiaki Department of Pathology, School of Medicine, The University of Tokushima Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Komagata, Yoshinori Institute of Development, Aging and Cancer, Tohoku University
Miyazaki, Jun-Ichi Department of Nutrition and Physiological Chemistry, Osaka University
Kikutani, Hitoshi Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University
Itakura, Mitsuo Division of Genetic Information, Institute for Genome Research, The University of Tokushima Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Keywords
nonobese diabetic (NOD) mice
pancreatic islets
rat glucagon promoter (RGP)
adoptive transfer
CD4+ and CD8+ T cells
Content Type
Journal Article
Description
Paracrine effect of transforming growth factor-β1 (TGF-β1) on autoimmune insulitis and diabetes was studied by transgenic production of the active form of porcine TGF-β1 (pTGF-β1) in pancreatic islet (islet) α cells in nonobese diabetic (NOD) mice under the control of rat glucagon promoter (RGP) (NOD-RGP-TGF-β1). None of 27 NOD-RGP-TGF-β1 mice developed diabetes by 45 wk of age, in contrast to 40 and 71% in male and female nontransgenic mice, respectively. None of the NOD-RGP-TGF-β1 mice developed diabetes after cyclophosphamide (CY) administration. Adoptive transfer of splenocytes of NOD-RGP-TGF-β1 mice to neonatal NOD mice did not transfer diabetes after CY administration. Adoptive transfer of three types of diabetogenic lymphocytes to NOD-RGP-TGF-β1 and nontransgenic mice after CY administration led to the lower incidence of diabetes in NOD-RGP-TGF-β1 mice versus that in nontransgenic mice: 29 vs. 77% for diabetogenic splenocytes, 25 vs. 75% for islet β cell–specific Th1 clone cells, and 0 vs. 50% for islet β cell–specific CD8+ clone cells, respectively. Based on these, it is concluded that autoimmune diabetes in NOD mice is not a systemic disease and it can be completely prevented by the paracrine TGF-β1 in the islet compartment through protection against CD4+ and CD8+ effector lymphocytes.
Journal Title
Journal of Clinical Investigation
ISSN
00219738
NCID
AA00695520
Volume
102
Issue
3
Start Page
499
End Page
506
Sort Key
499
Published Date
1998-08
Remark
© The American Society for Clinical Investigation, Inc.
EDB ID
Published Source
Journal of Clinical Investigation (1998) Vol.102 No.3 p.499–506
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher
departments
Oral Sciences
Medical Sciences
Institute of Advanced Medical Sciences
University Hospital