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RIPK3は,細胞死による神経炎症によるウイルス病変を抑制する

Brian P Daniels¹, Annelise G Snyder¹, Tayla M Olsen¹

¹Department of Immunology, University of Washington, Seattle, WA 98109, USA.

|April 4, 2017

まとめ

受容体相互作用タンパク質キナーゼ3 (RIPK3) は,細胞死に関係なく,西ナイルウイルスの病原性を制限する. RIPK3は,ケモカイン発現と免疫細胞の徴集を調節することによって,中枢神経系 (CNS) 内での免疫反応を調整する.

科学分野:

免疫学
神経科学
ウイルス学

背景:

受容体相互作用タンパク質キナーゼ3 (RIPK3) は,死滅性細胞死を活性化することが知られている.
RIPK3は,細胞死とは無関係に炎症シグナル伝達にも役割を果たします.
ネクロプトーシスは抗ウイルス免疫に寄与するが,宿主防御におけるRIPK3の死亡独立の役割は不明である.

研究の目的:

西ナイルウイルス (WNV) 感染に対する宿主防御におけるRIPK3の役割を調査する.
RIPK3が細胞死活性化機能とは無関係に WNVの病原性を抑制するかどうかを判断する.

主な方法:

西ナイルウイルス (WNV) の脳炎のマウスモデルを使用した.
野生型 (WT) のマウス,Ripk3ノックアウト (Ripk3-/-) のマウス,およびネクロプトーシス効果因子 (MLKLまたはMLKLおよびカスペーゼ-8) を欠いたマウスの死亡率と免疫応答の比較.
中枢神経系 (CNS) のケモカイン発現と免疫細胞の浸透を評価した.

主要な成果:

Ripk3-/- マウスはWT対照群と比較して死亡率が増加した.
MLKLまたはMLKLとカスパース8の両方が欠けていたマウスは影響を受けず,RIPK3が死亡に独立する役割を示した.
Ripk3- / - マウスにおける感受性の向上は,神経ケモカイン発現抑制と,中枢神経のTリンパ球と骨髄細胞の徴集減少と関連していた.
Ripk3- / - マウスでは周辺免疫が保たれた.

結論:

RIPK3は,死滅性細胞死に関係なく,WNVの病原性を抑制する.
RIPK3は,ウイルスの病原性を制限するプレオトロプ的機能を果たしている.
RIPK3は,ウイルス性脳炎における中枢神経内部の免疫反応の重要な調整者です.

キーワード:

RIPK1 について RIPK3 について西ナイルウイルスケモカインネクロプトーシス神経免疫学神経炎症

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