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関連する概念動画

The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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このページは機械翻訳されています。他のページは英語で表示される場合があります。View in English
  1. ホーム
  3. 研究分野
  5. 生物医学と臨床科学
  7. 心血管医学と血液学
  9. 心臓病 (心血管疾患を含む)
  11. Jak- Statシグナリングの抑制は,中型および大型血管炎における病原性免疫反応を抑制する.

JAK- STATシグナリングの抑制は,中型および大型血管炎における病原性免疫反応を抑制する.

Hui Zhang1, Ryu Watanabe1, Gerald J Berry2

  • 1Department of Medicine, Division of Immunology and Rheumatology (H.Z., R.W., J.J.G., C.M.W.).

Circulation
|December 20, 2017

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PubMed で要約を見る

まとめ
この要約は機械生成です。

ジャヌスキナーゼ (JAK) 阻害剤であるトファシチニブは,T細胞を標的とし,血管損傷を減らすことで,巨細胞動脈炎の慢性炎症を効果的に抑制します. この治療法では 組織内にある記憶T細胞を最小限に抑え 血管炎を誘発する主要な経路を阻害します

科学分野:

  • 免疫学
  • 心血管医学
  • リウマトロジ

背景:

  • 巨細胞動脈炎 (GCA) は慢性的な自己免疫性血管炎で,大動脈に影響し,動脈瘤や閉塞などの合併症を引き起こします.
  • GCAの持続的な炎症は,エフェクターT細胞と組織内記憶T細胞を巻き込み,コルチコステロイド治療にもかかわらず慢性血管炎に寄与する.
  • 炎症は微小血管新生と 内臓増殖を引き起こし 動脈の整合性を損なう

研究 の 目的:

  • 組織内定の記憶T細胞を含む損傷T細胞が,GCAで持続的な炎症を維持するかどうかを調査する.
  • JAK3とJAK1を標的とするジャヌスキナーゼ (JAK) 阻害剤であるトファシチニブに対するこれらのT細胞の感受性を決定する.

主な方法:

  • GCA患者の人の動脈を免疫欠乏症のマウスに埋め込み,患者の免疫細胞で復元した.
  • 炎症した動脈を持つマウスは,トファシチニブまたはベクチュール・コントロールで治療した.
  • 血管炎症,遺伝子/タンパク質発現,免疫細胞集団はRT-PCR,免疫ヒストケミストリー,フロー細胞測定を用いて分析された.

主要な成果:

  • トファシチニブは,動脈壁内の先天性および適応性免疫を著しく抑制しました.
  • 損傷T細胞の増殖とエフェクタ分子 (IFN-γ,IL-17,IL-21) の生成がトファシチニブ治療で減少した.
キーワード:
ジャヌスキナーゼSTATの転写因子Tリンパ球サイトカイン

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  • トファシチニブは,アドベンチアル血管新生を抑制し,内臓増殖を減少させ,CD4+CD103+組織内記憶T細胞を減少させた.

    • 結論:

    • GCAの影響を受けた大動脈の慢性炎症には,JAK3とJAK1によるサイトカインシグナル伝達が不可欠です.
    • JAK阻害剤トファシチニブは,組織内定の記憶T細胞とGCAにおける主要な血管新生経路を効果的に抑制する.
    • トファシチニブは,GCAにおける慢性動脈炎症の管理のための治療薬としての可能性を示しています.
    巨大細胞動脈炎
    炎症
    血管炎