感染症はT細胞の耐性を破る
M Röcken1, J F Urban, E M Shevach
1Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892.
Nature
|September 3, 1992
まとめ
Nippostrongylus brasiliensisの感染は,Staphylococcus enterotoxin B (SEB) によって確立されたT細胞耐性を破ることができます. これは,感染症剤が,アナーギー性T細胞を活性化することによって,自己免疫疾患を誘発する可能性があることを示唆しています.
科学分野:
- 免疫学 免疫学とは
- 自己免疫とは,自己免疫である.
- 感染症 感染症とは
背景:
- T細胞の耐性は,クローン欠損またはアナージーによって確立され,自己免疫反応を防ぐ.
- 自動反応性T細胞は,通常,自己耐性を維持するために抑制されます.
研究 の 目的:
- 併発感染が確立されたT細胞耐性を破るかどうかを調査する.
- 感染剤がT細胞耐性を回避するメカニズムを特定する.
主な方法:
- Staphylococcus enterotoxin B (SEB) を使用したマウスにおけるT細胞耐性の誘導.
- 耐性のあるT細胞をSEBで試験管内でテストし,サイトカインの産生 (インタールイキン-2,インタールイキン-4) を評価する.
- 耐性のあるマウスをニポストロンギルス (Nippostrongylus brasiliensis) というネマトードに感染させ,T細胞の反応を in vivo で分析した.
主要な成果:
- SEB耐性T細胞は,インビトロSEBチャレンジでインタールイキン-2または-4を産生しなかった.
- SEB耐性マウスのN. brasiliensis感染は,耐性T細胞の正常な拡張につながった.
- 感染はまた,耐性および正常な動物の両方で,SEB反応性,インタールイキン-4生成T細胞の増加をもたらしました.
結論:
- Nippostrongylus brasiliensisの感染は,SEBが誘発したT細胞の耐性を効果的に回避する.
- 感染症剤は,代替経路を通じて無性T細胞を活性化することで,自己免疫を誘発する可能性があります.
- この研究は,自己免疫疾患の発症における感染性トリガーの潜在的なメカニズムを強調しています.
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