PYNOD (NLR ファミリーに属する細胞質蛋白)の欠損マウスを作成し、主に免疫系におけるPYNODの役割を検討した。PYNOD欠損マウスの自然免疫応答に明確な異常は認められず、獲得免疫応答である遅延型過敏症応答に異常が認められた。しかし、皮膚経路で免疫したマウスの所属リンパ節は正常な抗原特異的インターフェロンγ産生能を示し、末梢組織に投与した抗原が所属リンパ節に到達し、エフェクターT細胞が生成されるプロセスは正常であることが示唆された。したがって、PYNOD欠損マウスの獲得免疫応答異常の原因は所属リンパ節のエフェクターT細胞が末梢組織へ移動する段階以降に存在することが示唆された。
In this study, we have investigated the physiological role of PYNOD (a cytoplasmic protein belonging to the NLR family), especially its role in the immune system using PYNOD-deficient mice. PYNOD-deficient mice exhibited a clear defect in the delayed type hypersensitivity that is a type of acquired immune responses, whereas we could find no apparent defect in innate immune responses in these mice. However, draining lymph node cells isolated from PYNOD-deficient mice that had been immunized through skin routes exhibited normal antigen-specific IFN-gamma production, suggesting that peripheral antigen was successfully delivered to draining lymph nodes and effecter T cells were normally generated in these mice. Thus, it is likely that the cause of the defect in the acquired immune system of PYNOD-deficient mice exist in a process of or after the migration of effecter T cells from draining lymph nodes to peripheral tissues.
炎症抑制型NLR蛋白PYNODの生理的・病理的役割の解明
.png)
CA-PR-SUDA-T-kaken 2014-4p.pdf
(98.3KB)
