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
102
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
72187
出典
Journal of Clinical Investigation (1998) Vol.102 No.3 p.499–506
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