1 型糖尿病 の 遺伝 的 危険因子
Flemming Pociot1, Åke Lernmark2
1Department of Pediatrics, Herlev and Gentofte Hospital, DK-2730 Herlev, Denmark.
Lancet (London, England)
|June 16, 2016
まとめ
1型糖尿病はベータ細胞の自己免疫期間を経て発症し,しばしば複数の自己抗体によって引き起こされます. より多くの自己抗体型は,病原性のバイオマーカーとして機能し,病気の急速な進行のリスクを高めます.
科学分野:
- 免疫学
- 内分泌学
- 遺伝学
背景:
- 1型糖尿病 (T1D) の診断はベータ細胞自身免疫のプロドロマの段階に続く.
- インスリンに対する自己抗体,グルタミン酸デカルボキシラーゼ (GAD),島根抗原-2 (IA-2),ZnT8トランスポーターは重要なバイオマーカーです.
- 遺伝的傾向,特にHLA-DR3-DQ2およびHLA-DR4-DQ8ハプロタイプは,主要な危険因子です.
研究 の 目的:
- 1型糖尿病の病原性における自己抗体の役割を解明する.
- 自己抗体プロファイルと疾患の進行の関係を理解する.
- 1型糖尿病を他の臓器特異性自己免疫疾患のモデルとして検討する.
主な方法:
- 1型糖尿病患者の自己抗体の存在とタイプを分析する.
- 自己抗体プロファイルと遺伝的リスク因子 (HLAハプロタイプ) の相関
- 自己免疫性,血糖制御,および症状に基づく疾患の発症段階.
主要な成果:
- 多数のベータ細胞自己抗体の存在は,1型糖尿病の急速な進行のリスクと相関しています.
- オートアンチボディは,根底にある自己免疫プロセスの再現可能なバイオマーカーとして機能する.
- 遺伝的に感受性の高い個体において,環境的トリガーは一般的に必要である.
結論:
- 1型糖尿病の進行を予測する重要な要因である.
- 1型糖尿病の病原性は,遺伝的関連が異なる異なる段階に分けられる.
- T1Dは,長時間の臨床前段階を持つ他の自己免疫疾患の研究に価値のあるモデルとして機能します.
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