Abrogation of Autoimmune Diabetes in Nonobese Diabetic Mice and Protection against Effector Lymphocytes by Transgenic Paracrine TGF-β1

Moritani, Maki; Yoshimoto, Katsuhiko; Wong, Susan F.; Tanaka, Chisato; Yamaoka, Takashi; Sano, Toshiaki; Komagata, Yoshinori; Miyazaki, Jun-ichi; Kikutani, Hitoshi; Itakura, Mitsuo

doi:https://doi.org/10.1172/JCI2992

Abrogation of Autoimmune Diabetes in Nonobese Diabetic Mice and Protection against Effector Lymphocytes by Transgenic Paracrine TGF-β1

Moritani, Maki; Yoshimoto, Katsuhiko; Wong, Susan F. et al.

Journal of Clinical Investigation, 1998, 102(3), 499-506

アクセス数:1,154件（2026-02-10 14:38 集計）

固定URL: https://hdl.handle.net/11094/23116

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タイトル	Abrogation of Autoimmune Diabetes in Nonobese Diabetic Mice and Protection against Effector Lymphocytes by Transgenic Paracrine TGF-β1
著者	NRID 1000050301312 1000050301312 著者名 Moritani, Maki
	NRID 1000020271257 1000020271257 著者名 Yoshimoto, Katsuhiko
	著者名 Wong, Susan F.
	著者名 Tanaka, Chisato
	NRID 1000040263826 1000040263826 著者名 Yamaoka, Takashi
	NRID 1000080154128 1000080154128 著者名 Sano, Toshiaki
	NRID 1000060281995 1000060281995 著者名 Komagata, Yoshinori
	NRID 1000080229830 1000080229830 著者名 Miyazaki, Jun-ichi
	NRID 1000080161412 1000080161412 著者名 Kikutani, Hitoshi
	NRID 1000060134227 1000060134227 著者名 Itakura, Mitsuo
キーワード等	nonobese diabetic (NOD) mice
	pancreatic islets
	rat glucagon promoter (RGP)
	adoptive transfer
	CD4^+ and CD8^+ T cells
抄録	Paracrine effect of transforming growth factor-beta1 (TGF-beta1) on autoimmune insulitis and diabetes was studied by transgenic production of the active form of porcine TGF-beta1 (pTGF-beta1) in pancreatic islet (islet) alpha cells in nonobese diabetic (NOD) mice under the control of rat glucagon promoter (RGP) (NOD-RGP-TGF-beta1). None of 27 NOD-RGP-TGF- beta1 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-beta1 mice developed diabetes after cyclophosphamide (CY) administration. Adoptive transfer of splenocytes of NOD-RGP-TGF-beta1 mice to neonatal NOD mice did not transfer diabetes after CY administration. Adoptive transfer of three types of diabetogenic lymphocytes to NOD-RGP-TGF-beta1 and nontransgenic mice after CY administration led to the lower incidence of diabetes in NOD-RGP-TGF-beta1 mice versus that in nontransgenic mice: 29 vs. 77% for diabetogenic splenocytes, 25 vs. 75% for islet beta cell-specific Th1 clone cells, and 0 vs. 50% for islet beta 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-beta1 in the islet compartment through protection against CD4^+ and CD8^+ effector lymphocytes.
出版者	American Society for Clinical Investigation
収録物名	Journal of Clinical Investigation
巻(号)	102(3)
ページ	499-506
刊行年月	1998-08
言語	英語
ハンドルURL	https://hdl.handle.net/11094/23116
PISSN	00219738
NCID	AA00695520
関連情報 (isIdenticalTo)	DOI (出版社版) https://doi.org/10.1172/JCI2992
アクセス権	open access
権利情報	Copyright © 1998, The American Society for Clinical Investigation
出版タイプ	Version of Record
カテゴリ	学術雑誌論文 Journal Article

資源タイプ	学術雑誌論文
ローカル資源タイプ	学術雑誌論文
DCMI資源タイプ	text
DCTERMS.bibliographicCitation	Journal of Clinical Investigation. 1998, 102(3), p. 499-506
DC.title	Abrogation of Autoimmune Diabetes in Nonobese Diabetic Mice and Protection against Effector Lymphocytes by Transgenic Paracrine TGF-β1
DC.creator	Moritani, Maki
	Yoshimoto, Katsuhiko
	Wong, Susan F.
	Tanaka, Chisato
	Yamaoka, Takashi
	Sano, Toshiaki
	Komagata, Yoshinori
	Miyazaki, Jun-ichi
	Kikutani, Hitoshi
	Itakura, Mitsuo
DC.publisher	American Society for Clinical Investigation
DC.language' scheme='DCTERMS.RFC1766	英語
DC.type' scheme='DCTERMS.DCMIType	text
DCTERMS.issued' scheme='DCTERMS.W3CDTF	1998-08
DC.identifier	https://doi.org/10.1172/JCI2992
DC.subject	nonobese diabetic (NOD) mice
	pancreatic islets
	rat glucagon promoter (RGP)
	adoptive transfer
	CD4^+ and CD8^+ T cells
DCTERMS.abstract	Paracrine effect of transforming growth factor-beta1 (TGF-beta1) on autoimmune insulitis and diabetes was studied by transgenic production of the active form of porcine TGF-beta1 (pTGF-beta1) in pancreatic islet (islet) alpha cells in nonobese diabetic (NOD) mice under the control of rat glucagon promoter (RGP) (NOD-RGP-TGF-beta1). None of 27 NOD-RGP-TGF- beta1 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-beta1 mice developed diabetes after cyclophosphamide (CY) administration. Adoptive transfer of splenocytes of NOD-RGP-TGF-beta1 mice to neonatal NOD mice did not transfer diabetes after CY administration. Adoptive transfer of three types of diabetogenic lymphocytes to NOD-RGP-TGF-beta1 and nontransgenic mice after CY administration led to the lower incidence of diabetes in NOD-RGP-TGF-beta1 mice versus that in nontransgenic mice: 29 vs. 77% for diabetogenic splenocytes, 25 vs. 75% for islet beta cell-specific Th1 clone cells, and 0 vs. 50% for islet beta 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-beta1 in the islet compartment through protection against CD4^+ and CD8^+ effector lymphocytes.
DC.rights	Copyright © 1998, The American Society for Clinical Investigation
DC.format	23116
citation_title	Abrogation of Autoimmune Diabetes in Nonobese Diabetic Mice and Protection against Effector Lymphocytes by Transgenic Paracrine TGF-β1
citation_author	Moritani, Maki
	Yoshimoto, Katsuhiko
	Wong, Susan F.
	Tanaka, Chisato
	Yamaoka, Takashi
	Sano, Toshiaki
	Komagata, Yoshinori
	Miyazaki, Jun-ichi
	Kikutani, Hitoshi
	Itakura, Mitsuo
citation_publisher	American Society for Clinical Investigation
citation_language	英語
citation_date	1998-08
citation_journal_title	Journal of Clinical Investigation
citation_volume	102
citation_issue	3
citation_firstpage	499
citation_lastpage	506
citation_doi	https://doi.org/10.1172/JCI2992
citation_public_url	https://hdl.handle.net/11094/23116

Abrogation of Autoimmune Diabetes in Nonobese Diabetic Mice and Protection against Effector Lymphocytes by Transgenic Paracrine TGF-β1

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