腸内微生物のミミックは,糖尿病を誘発する自己反応性を奪い,大腸炎を抑制する
Roopa Hebbandi Nanjundappa1, Francesca Ronchi2, Jinguo Wang1
1Julia McFarlane Diabetes Research Centre (JMDRC), University of Calgary, Calgary AB T2N 4N1, Canada; Department of Microbiology, Immunology, and Infectious Diseases, Snyder Institute for Chronic Diseases, University of Calgary, Calgary AB T2N 4N1, Canada.
Cell
|October 21, 2017
まとめ
腸内細菌は免疫に 影響を及ぼします バクテロイドの統合酵素は自己抗原を模倣し,分子模倣によって腸内炎症を抑制するためにT細胞を募集します.
科学分野:
- 免疫学
- 微生物学
- 胃腸内科
背景:
- 腸内微生物群は 免疫の発達に不可欠です
- 微生物の調節不良は 自己免疫を引き起こす可能性があります
- 抗原特異的でない免疫効果は病気に関与している.
研究 の 目的:
- 免疫調節におけるバクテロイド・インテグラーゼの役割を調査する.
- 微生物成分が自己抗原を真似できるかどうかを判断する.
- 炎症性疾患における腸内微生物の治療の可能性を探求する.
主な方法:
- 細菌のないマウスは 改造されたバクテロイド種で 植え付けられました
- T細胞の募集と機能を分析した.
- 分子模倣と免疫抑制メカニズムが研究されました.
主要な成果:
- バクテロイドス・インテグラーゼは,IGRP206-214のミモトープとして作用する.
- 微生物のエピトープは 糖尿病性CD8+T細胞を腸に誘導する.
- これらのT細胞は特定の免疫経路を通して大腸炎を抑制します.
- 人間のT細胞はバクテロイド・インテグラーゼを認識する
結論:
- 腸内微生物の抗原特異性T細胞は,炎症性腸疾患を治療することができる.
- 腸内微生物による 分子模倣は 新しい免疫調節メカニズムです
- バクテロイド・インテグラーゼは免疫ホメオスタシスを影響する.
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