IL-12 plays a pathologic role at the inflammatory loci in the development of diabetes in NOD mice

Yoshio Nitta, Shunsuke Kawamoto, Fumi Tashiro, Hiroyuki Aihara, Takayuki Yoshimoto, Hideo Nariuchi, Koichi Tabayashi, Jun Ichi Miyazaki

研究成果: Article査読

25 被引用数 (Scopus)

抄録

Accumulating evidence suggests that CD4+ T helper type 1 (Th1) cells play a major role in the development of insulin-dependent diabetes mellitus (IDDM) in the non-obese diabetic (NOD) mouse model. Interleukin (IL)-12 is a potent immunoregulatory molecule that is a key determinant of T-cell differentiation into Th1 cells, and has been implicated in the development of IDDM. To investigate the role of IL-12 that is locally produced by islet-infiltrating cells in the development of IDDM, we generated transgenic NOD mice in which the IL-12 p40 homodimer, a natural antagonist of IL-12, was produced exclusively in islets without affecting the levels of IL-12 p40 in the systemic circulation. We found that the incidence of diabetes was significantly reduced in these transgenic mice. These results clearly demonstrate that IL-12 locally produced by islet-infiltrating cells plays a critical role in the development of IDDM.

本文言語English
ページ(範囲)97-104
ページ数8
ジャーナルJournal of Autoimmunity
16
2
DOI
出版ステータスPublished - 2001
外部発表はい

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学

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