葉っぱの調節性T細胞は,B細胞を調節するためにニューリチンを産生する

Paula Gonzalez-Figueroa¹, Jonathan A Roco¹, Ilenia Papa¹

¹Dept of Immunology and Infectious Disease, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT, Australia.

Cell

|March 12, 2021

まとめ

葉っぱの調節性T細胞は,B細胞の過剰活性化を防ぐタンパク質であるニューリチンを産生する. この発見は自己免疫とアレルギーを抑制する重要なメカニズムを明らかにしています

科学分野:

免疫学
細胞生物学

背景:

調節性T細胞 (Tregs) は免疫ホメオスタシスに不可欠です.
Tregsが自己抗体と過剰なIgEを防ぐ正確なメカニズムは,まだ完全に理解されていません.

研究の目的:

免疫調節におけるBCL6発現するTレグ,特に卵泡調節性T (Tfr) 細胞の役割を明らかにする.
Tfr細胞によって生成されるニューリチンタンパク質が,B細胞の反応を制御する機能を調査する.

主な方法:

Foxp3発現する細胞にTfr細胞やニューリチンが欠けているマウスの分析.
免疫接種時の自己抗体産生,IgEおよびIgG1レベルの評価
クラス交換と分化を含むニューリチン吸収とB細胞への影響の調査.
転写因子BCL6とBLIMP-1に対するニューリチンの影響の評価
Tfr欠乏したマウスにニューリチンの実験投与

主要な成果:

Tfr細胞やニューリチンが欠けていたマウスは,早期に血細胞を蓄積し,自己抗体を発達させた.
これらのマウスはワクチン接種後,血IgEとIgG1が増加した.
ニューリチンはB細胞によって内化され,タンパク質のリン酸化とIgEクラスの切り替えが減少することが判明した.
ニューリチンは生殖中心のB細胞の分化を阻害し,BLIMP- 1を低下させ,BCL- 6を上昇させました.
ニューリチンの投与は,Tfr欠乏したマウスの血細胞の蓄積を逆転させた.

結論:

Tfr細胞によって産生されるニューリチンは,B細胞の過活性を抑制する重要な媒介です.
このTfr細胞由来ニューリチンの経路は,B細胞主導の自己免疫およびIgE媒介のアレルギーの予防に不可欠です.

キーワード:

IgE についてオートアンチボディ自己免疫性卵泡ヘルパーT (Tfh)卵泡の調節性T (Tfr)発芽センター (GC)ニューリチン

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