The role of Tyk2, Stat1 and Stat4 in LPS-induced endotoxin signals

Kenjirou Kamezaki, Kazuya Shimoda, Akihiko Numata, Tadashi Matsuda, Kei Ichi Nakayama, Mine Harada

研究成果: ジャーナルへの寄稿学術誌査読

76 被引用数 (Scopus)

抄録

Mice lacking Tyk2, Stat1 or Stat4, which are members of the Jak-Stat signaling cascade, were resistant to LPS-induced endotoxin shock. Interestingly, Tyk2-deficient mice had higher resistance to LPS challenge than mice lacking either Stat1 or Stat4. The activation of MAPK and NF-κB by LPS, and the production of TNF-α and IL-12 after LPS injection, were not abrogated by the absence of Tyk2, Stat1 or Stat4 In Stat1-deficient mice, the induction of IFN-β by LPS in macrophages was severely reduced, although the serum level of IFN-γ was elevated after LPS injection. In contrast, in Stat-4 deficient mice, the induction of IFN-β by LPS was normal, but the serum level of IFN-γ remained low after LPS injection. Interestingly, the induction of both IFN-β and IFN-γ by LPS was severely reduced in Tyk2-deficient mice. Therefore, Stat1 and Stat4 independently play substantial roles in the susceptibility to LPS. Tyk2 is essential for LPS-induced endotoxin shock, and this signaling pathway is transduced by the activation of Stat1 and Stat4.

本文言語英語
ページ(範囲)1173-1179
ページ数7
ジャーナルInternational immunology
16
8
DOI
出版ステータス出版済み - 8月 2004
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 免疫アレルギー学
  • 免疫学

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