胰島はリンパ性組織とインスリンペプチドのエクソサイトーシスを通して通信する
Xiaoxiao Wan1, Bernd H Zinselmeyer1, Pavel N Zakharov1
1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, USA.
Nature
|July 20, 2018
まとめ
臓の小島細胞は T細胞が認識する 分解されたインスリン断片を放出し 自己免疫型の1型糖尿病を引き起こします この自己認識の経路は組織特有の自己免疫がどのように発達するのかを強調し,治療的介入のターゲットを提供します.
科学分野:
- 免疫学
- 内分泌学
- 自己免疫性
背景:
- 組織特異的自己免疫には,MHC分子によって提示される自己抗原のT細胞認識が含まれます.
- 自免疫性における支配的な自己抗原反応を駆動する正確なメカニズムは不明である.
- インスリン投与は,肥満でない糖尿病マウスの自己免疫型糖尿病の発症に不可欠です.
研究 の 目的:
- CD4 T細胞によるインスリンエピトープの分布と認識を調査する.
- 臓のベータ細胞の粒子の内にある分解されたインスリン断片を特定する.
- 1型糖尿病につながる 自己認識の経路を解明する
主な方法:
- リンパ節におけるCD4T細胞のインスリン認識の生画像
- ベータ細胞の粒子のインスリンペプチド断片を特定するための質量スペクトロメトリ.
- 特定のインスリンエピトープに対するT細胞反応の分析 (B:12‐20 vs. B:13‐21)
主要な成果:
- 病原性CD4T細胞はインスリンB:12-20エピトープを認識し,胸膜陰性選択を逃れる.
- 病原性エピトープを含む,分解されたインスリン断片は,ベータ細胞の粒の中に見つかる.
- グルコースチャレンジはこれらの断片を放出し,全身のCD4T細胞活性化と糖尿病発生性を高めます.
結論:
- 臓の小島は分解されたインスリンを放出し,自己耐性を常に脅かします.
- この研究は1型糖尿病における 主要な自己抗原の自己認識経路を明らかにした.
- 発見は,全身の自己免疫を促進する抗原標的を特定するための基礎を提供します.
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