ID | 109647 |
著者 |
モリタニ, マキ
Otsuka Department of Clinical and Molecular Nutrition, School of Medicine, The University of Tokushima
吉本, 勝彦
Otsuka Department of Clinical and Molecular Nutrition, School of Medicine, The University of Tokushima
徳島大学 教育研究者総覧
KAKEN研究者をさがす
Wong, Susan F.
Section of Immunobiology, Yale University School of Medicine
田中, 知里
Otsuka Department of Clinical and Molecular Nutrition, School of Medicine, The University of Tokushima
KAKEN研究者をさがす
ヤマオカ, タカシ
Otsuka Department of Clinical and Molecular Nutrition, School of Medicine, The University of Tokushima
佐野, 壽昭
Department of Pathology, School of Medicine, The University of Tokushima
徳島大学 教育研究者総覧
KAKEN研究者をさがす
コマガタ, ヨシノリ
Institute of Development, Aging and Cancer, Tohoku University
ミヤザキ, ジュンイチ
Department of Nutrition and Physiological Chemistry, Osaka University
キクタニ, ヒトシ
Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University
板倉, 光夫
Division of Genetic Information, Institute for Genome Research, The University of Tokushima
徳島大学 教育研究者総覧
KAKEN研究者をさがす
|
キーワード | nonobese diabetic (NOD) mice
pancreatic islets
rat glucagon promoter (RGP)
adoptive transfer
CD4+ and CD8+ T cells
|
資料タイプ |
学術雑誌論文
|
抄録 | 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.
|
掲載誌名 |
Journal of Clinical Investigation
|
ISSN | 00219738
|
cat書誌ID | AA00695520
|
巻 | 102
|
号 | 3
|
開始ページ | 499
|
終了ページ | 506
|
並び順 | 499
|
発行日 | 1998-08
|
備考 | © The American Society for Clinical Investigation, Inc.
|
EDB ID | |
出版社版DOI | |
出版社版URL | |
フルテキストファイル | |
言語 |
eng
|
著者版フラグ |
出版社版
|
部局 |
歯学系
医学系
先端酵素学研究所
病院
|