人間 の 適応 免疫 は 生まれつき の 免疫 の 誤り を 解き放つ
Laura Israel1, Ying Wang2, Katarzyna Bulek3
1Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, 75015 Paris, France; Paris Descartes University, Imagine Institute, 75015 Paris, France.
Cell
|February 25, 2017
まとめ
単発性疾患における不完全な浸透は,得られた抗体によって説明される. 遺伝的なTIRAP欠乏症は,LTA特異性抗体が欠けている場合にのみ,スタフィロコック病を引き起こす.
科学分野:
- 免疫学
- 遺伝学
- 感染症
背景:
- モノジェニック障害は,分子レベルで完全に理解されていない現象である,不完全な浸透性をしばしば表します.
- トール型受容体 (TLR) 媒介の免疫は,Staphylococcusのような細菌病原体に対する防御に不可欠です.
- TIRAP (Toll-interleukin 1受容体ドメインを含むアダプタータンパク質) は,TLRシグナル伝達に不可欠である.
研究 の 目的:
- 自体逆行型TIRAP欠乏症における不完全な浸透性の分子基礎を調査する.
- TIRAPと獲得した抗体が, stafilococcal感染に対する感受性における役割を理解する.
主な方法:
- TIRAP欠乏症の8人の関係者を研究した.
- 患者の線維細胞と白血球におけるトール型受容体アゴニストに対する細胞反応を評価した.
- 患者およびマウスモデルにおける免疫反応に対する抗リポテイホー酸 (LTA) モノクローナル抗体 (mAb) の効果を調査した.
主要な成果:
- すべてのTIRAP欠乏症患者は,TLR1/ 2,TLR2/ 6,TLR4アゴニストに対する反応が低下した.
- LTA特異性抗体 (Abs) を欠いた試薬のみが,TLR2/ 6アゴニストLTAに対する全血反応の完全な欠如を示した.
- TIRAP欠乏症の個人およびマウスの獲得した抗LTAAbsによるTLR2依存免疫は,TLR2またはMyD88に依存する効果である.
結論:
- 遺伝的TIRAP欠乏症の個体において,得られた抗LTAAbsはTLR2依存の免疫を回復させ,不完全な浸透性を説明する.
- TIRAPと抗LTA Abの欠乏症の組み合わせは,試薬における重症なスタフィロコック病の原因である.
- この研究は,遺伝的な免疫欠陥と,病気の病原性における得られた体内免疫の相互作用を強調しています.
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