Hyperproduction of Proinflammatory Cytokines by WSX-1-Deficient NKT Cells in Concanavalin A-Induced Hepatitis

Atsushi Yamanaka, Shinjiro Hamano, Yoshiyuki Miyazaki, Kazunari Ishii, Atsunobu Takeda, Tak W. Mak, Kunisuke Himeno, Akihiko Yoshimura, Hiroki Yoshida

研究成果: Contribution to journalArticle査読

77 被引用数 (Scopus)

抄録

Administration of Con A induces liver injury that is considered to be an experimental model for human autoimmune or viral hepatitis, where immunopathology plays roles mediated by activated lymphocytes, especially NK1.1+ CD3+ NKT cells, and inflammatory cytokines, including IFN-γ and IL-4. In the present study we investigated the role of WSX-1, a component of IL-27R, in Con A-induced hepatitis by taking advantage of WSX-1 knockout mice. WSX-1-deficient mice were more susceptible to Con A treatment than wild-type mice, showing serum alanine aminotransferase elevation and massive necrosis in the liver. Although the development of NKT cells appeared normal in WSX-1 knockout mice, purified NKT cells from the knockout mice produced more IFN-γ and IL-4 than those from wild-type mice in response to stimulation with Con A both in vitro and in vivo. In addition, hyperproduction of proinflammatory cytokines, including IL-1, IL-6, and TNF-α, was observed in the knockout mice after Con A administration. These data revealed a novel role for WSX-1 as an inhibitory regulator of cytokine production and inflammation in Con A-induced hepatitis.

本文言語英語
ページ(範囲)3590-3596
ページ数7
ジャーナルJournal of Immunology
172
6
DOI
出版ステータス出版済み - 3 15 2004

All Science Journal Classification (ASJC) codes

  • 免疫アレルギー学
  • 免疫学

フィンガープリント

「Hyperproduction of Proinflammatory Cytokines by WSX-1-Deficient NKT Cells in Concanavalin A-Induced Hepatitis」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル