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IL-35を産生するB細胞は,自己免疫疾患や感染症の際に免疫の重要な調節因子です

Ping Shen¹, Toralf Roch¹, Vicky Lampropoulou¹

¹Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Charitéplatz 1, 10117 Berlin, Germany.

|February 28, 2014

まとめ

インタールイキン-35 (IL-35) を生成するB細胞は,免疫調節に不可欠です. それらの欠如は,自己免疫疾患からの回復を阻害しますが,細菌感染症に対する耐性を高め,IL-35を治療目標として明らかにします.

科学分野:

免疫学免疫学とは
細胞生物学細胞生物学

背景:

B型リンパ球は,サイトカインの産生を通じて免疫反応を調節する.
B細胞からのインターリューキン-10 (IL-10) は,自己免疫を抑制するが,病原体の感受性を高めることが知られている.
免疫調節における他のB細胞由来サイトカインの役割については,さらなる解明が必要である.

研究の目的:

免疫応答の調節においてB細胞によって生成されるインタールイキン-35 (IL-35) の役割を調査する.
自身免疫疾患および感染症モデルに対するIL-35欠乏B細胞の影響を決定する.

主な方法:

特にB細胞でIL-35発現が欠けている遺伝子組み換えマウスを利用した.
疾患の重症度と病原体のクリアランスを試験的な自己免疫性脳髄膜炎 (EAE) とサルモネラ・エンテリカ・セロヴァーチフィムリウム感染モデルで評価した.
免疫細胞集団,活性化マーカー,およびサイトカインプロフィールを分析した.

主要な成果:

B細胞由来IL-35が欠けていたマウスは,EAEからの回復が低下したが,サルモネラ感染に対する抵抗性が強化された.
IL-35の欠如により,マクロファージとT細胞の活性化が増加し,B細胞抗原を提示する細胞の機能が改善されました.
IL-35とIL-10の生成は,主にプラズマ細胞の異なるサブセットと関連していました.

結論:

B細胞に由来するIL-35は,免疫の負の調節において重要な役割を果たします.
IL-35を産生するB細胞は,EAEのような自己免疫疾患の制御に重要である.
B細胞によるIL-35産生をターゲットにすることで,自己免疫性および感染症に対する潜在的な治療戦略が提供されます.

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