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エピテリアのIL-18均衡は,大腸炎におけるバリア機能を制御する

Roni Nowarski1, Ruaidhrí Jackson1, Nicola Gagliani1

  • 1Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.

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|December 7, 2015
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まとめ
この要約は機械生成です。

インタールイウキン18 (IL-18) は,腸内障壁を破壊することで潰瘍性大腸炎を誘発する. 腸内皮質細胞のIL-18シグナル伝達を遮断することで,大腸炎から保護し,コップレット細胞を保存します.

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科学分野:

  • 胃腸内科
  • 免疫学
  • 細胞生物学

背景:

  • 腸内粘膜壁は 微生物群の制御に不可欠で 粘液を生成するコップレット細胞に依存しています
  • 炎症性腸疾患,特に潰瘍性大腸炎の特徴は,小杯細胞機能の障害と粘液層の分解です.

研究 の 目的:

  • 大腸炎における腸壁の病理的崩壊におけるインタールイキン-18 (IL-18) の役割を調査する.
  • 腸内皮質細胞のIL-18シグナル伝達がコップレット細胞の成熟と大腸炎の重度に影響を与えるメカニズムを解明する.

主な方法:

  • 大腸炎のマウスモデルを使いました
  • 腸内皮質細胞におけるIl18,Il18r1 (IL-18受容体1) とIl18bp (IL-18結合タンパク質) の特定の欠損を有する遺伝子組み換えマウスを生成した.
  • 大腸炎の重症度,粘膜損傷,および組織学的および分子分析によるコップレット細胞の成熟を評価した.

主要な成果:

  • 腸内皮質細胞におけるIl18またはIl18r1の除去は,大腸炎および粘膜損傷に対する有意な保護を与えました.
  • Il18bpの消去は重度の大腸炎と成熟したコップレット細胞の喪失につながった.
  • 腸内皮質細胞におけるIl18bpとIl18r1の同時消去は,大腸炎とコップレット細胞喪失を救出し,重要なレギュレータとして上皮質細胞におけるIL-18シグナル伝達を確認した.
  • IL - 18は,カプレット細胞の発達を制御する転写プログラムを変えることで,カプレット細胞の成熟を阻害することが判明した.

結論:

  • 腸内皮質細胞内のIL-18シグナリングは,大腸炎の病理学と腸壁機能障害の重要な要因です.
  • 腸内皮質細胞におけるIL-18シグナル伝達をターゲットにすることは,潰瘍性大腸炎の潜在的な治療戦略を表しています.
  • 性大腸炎におけるガブレット細胞機能不全に対処するために,ガブレット細胞発達のIL-18の調節を理解することが鍵となる.