感染症と免疫病の分子生物学と医学

• 研究課題/領域番号: 09CE2007
• 研究種目: 特別推進研究(COE)
• 配分区分: 補助金
• 研究機関: 大阪大学
• 研究代表者: 山西 弘一 (2003) 大阪大学, 医学系研究科, 教授 (10029811); 岸本 忠三 (1997-2002) 大阪大学, 医学系研究科, 総長 (10093402)
• 研究分担者: 審良 静男 大阪大学, 微生物病研究所, 教授 (50192919) ; 菊谷 仁 大阪大学, 微生物病研究所, 教授 (80161412) ; 木下 タロウ 大阪大学, 微生物病研究所, 教授 (10153165) ; 山西 弘一 大阪大学, 医学系研究科, 教授 (10029811) ; 清野 宏 大阪大学, 微生物病研究所, 教授 (10271032)
• 研究期間 (年度): 1997 – 2003
• 研究課題ステータス: 完了 (2003年度)
• 配分額: 2,712,000千円 (直接経費: 2,565,000千円、間接経費: 147,000千円); 2003年度: 390,000千円 (直接経費: 300,000千円、間接経費: 90,000千円); 2002年度: 247,000千円 (直接経費: 190,000千円、間接経費: 57,000千円); 2001年度: 470,000千円 (直接経費: 470,000千円); 2000年度: 370,000千円 (直接経費: 370,000千円); 1999年度: 435,000千円 (直接経費: 435,000千円); 1998年度: 410,000千円 (直接経費: 410,000千円); 1997年度: 390,000千円 (直接経費: 390,000千円)
• キーワード: GPIアンカー / PIG-V / Sema4A / sema6D / TLR / MyD88非依存症性経路 / gH-gL-gO / LANA / 感染症 / 免疫病 / サイトカイン / 自然免疫 / ヒトヘルペスウイルス6 / セマフォリン / Toll様レセプター / 粘膜免疫 / インターロイキン6 / ヒトヘルペルウイルス6 / CD40 / ヒトヘルペスウイルス

研究概要

(木下)1.ヒトのGPIアンカー生合成遺伝子群の解明に関し、PIG-Vが第2のマンノース転移酵素であること、PIG-Wがイノシトールへのアシル転移酵素であること、PGAP1がイノシトール・デアシラーゼであることを証明した。これにより、GPIアンカーが小胞体膜の細胞質側から内腔側へフリップするステップを除き、生合成の全ステップに働く遺伝子群が解明された。2.睡眠病トリパノソーマのGPIアンカー生合成遺伝子群の解明に関し、アンカーをタンパク質に付加するGPIトランスアミダーゼにヒトには存在しない2つのタンパク質(TTA1,TTA2)が必須であることを見いだした。これらのタンパク質は、睡眠病治療薬の標的に適している。
(菊谷)これまでクラスIVセマフォリンSema4AがTIM2を介してT細胞を刺激することを報告してきたが、本年度はSema4A欠損マウスを作成し、その解析からSema4Aが抗原特異的T細胞の分化、特にTh1細胞に必須であることを示した。また、新規クラスVIセマファリンSema6Dをクローニングし、Sema6Dがその受容体Plexin-A1を介して心内皮細胞の遊走を調節し、心臓形態形成に必須の役割を果たすことを明らかにした。さらに、Sema6Dは免疫系においても樹状細胞のサイトカイン産生を誘導するなどの生物活性を有することが明らかになった。
(審良)Toll Like Receptor(TLR)を介した細胞内シグナル伝達では、全てのTLRの炎症性サイトカインの誘導に必須のMyD88依存性経路と、TLR3,4を介しInterfron(IFN)-β,IFN誘導性遺伝子を誘導するMyD88非依存性経路が存在する。MyD88と同じTIRドメインを持つアダプター群のノックアウトマウスの作製、解析を行った。TIRAPはTLR2,4を介したMyD88依存性経路に関与していた。データベースから同定したTRIFはTLR3,4を介するMyD88非依存性経路に、TRAMはTLR4を介するMyD88依存性経路にだけかかわるアダプターであることを明らかにした。TLRを介したシグナルはアダプター群が制御しその特異性も規定していることがわかった。
(山西)1.ヒトヘルペスウイルス7(HHV7)U12遺伝子が機能的なβケモカインレセプターであることを明らかにした。これによりU12遺伝子産物が何らかのかたちで病態発症にかかわっていることが示唆された。ヒトヘルペスウイルス6(HHV6)variant AのgH-gL-gQがCD46と相互作用すること、HHV6 A U100遺伝子産物がgH-gLコンプレックスの形成因子の一つになっていることなどが明らかになった。Variant Aとvariant Bではウイルス粒子膜分子の形成が異なっており、これが感染細胞の特異性を決めているものと思われる。2.カポジ肉腫関連ヘルペスウイルス(KSHV)では、前初期遺伝子RTAがアポトーシスインデューサーであるにも関わらず、感染細胞ではXIAPの発現上昇によりこの機能が阻止されることを明らかにした。この機構にはORF57遺伝子産物と宿主細胞因子PCBP1が相互作用することにより、XIAP遺伝子のIRESの機能を上昇させることが主な理由であることを突き止めた。潜伏感染状態はウイルス遺伝子latency associated nuclear antigen(LANA)がヒストンメチラーゼSUV39H1と相互作用し、ゲノムをヘテロクロマチン化することにより誘導され、このことが潜伏感染での遺伝子発現プロファイルに強く関わっていることを明らかにした。

研究成果

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