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KAKEN_16K08847seika.pdf
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Download
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:86.7 KB
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:Oct 31, 2019 |
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クロマチン制御因子TRIM28による自己反応性Th17の抑制機構
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クロマチン セイギョ インシ TRIM28 ニ ヨル ジコ ハンノウセイ Th17 ノ ヨクセイ キコウ
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Kuromachin seigyo inshi TRIM28 ni yoru jiko hannōsei Th17 no yokusei kikō
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Regulation of self-reactive T cells by TRIM28
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竹馬, 俊介
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チクマ, シュンスケ
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Chikuma, Shunsuke
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慶應義塾大学・医学部 (信濃町) ・講師
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Research team head
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科研費研究者番号 : 50437208
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時藤, 夕紀子
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トキフジ, ユキコ
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Tokifuji, Yukiko
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Collaborator
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石田, 典仁
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イシダ, ノリヒト
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Ishida, Norihito
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Collaborator
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大倉, 千明
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オオクラ, チアキ
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Ōkura, Chiaki
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Collaborator
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2019
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科学研究費補助金研究成果報告書
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2018
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| Abstract |
皮膚抗原を認識、攻撃するＴＣＲトランスジェニックマウスに、TRIM28欠損マウスを交配し、TRIM28の免疫寛容における役割を調べた。TRIM28欠損Ｔ細胞は、皮膚特異的Ｔ細胞だけでなく、幅広くＴ細胞の活性化を抑制すること、これまでにわかっていた、Th17の抑制以外に、制御性制御性T細胞に必須の遺伝子発現を通じ、自己免疫の抑制機構を担うことが示唆された。Th17と制御性制御性T細胞は、ともに似たサイトカイン環境で分化することが知られ、TRIM28がこのバランスを制御して、多くの免疫疾患を抑制していることが考えられた。
We previouslly shpwed mice deficient for TRIM28 molecule on lymphocytes develop sponteneous autoimmunity. To examine TRIM28 function in autorecative T cells, we bred TRIM28 KO mice to skin-specific TCR transgenic mice. We found negative regulation of lymphocyte activation by TRIM28 was polyclonal, rather than antigen specific, and involves deregulation of regulatory T cell (Treg) gene expression and function. Since IL-17 producing helper T cell (Th17) and Treg develop in a similar pathway, the data suggested that TRIM28 prevention of autoimmunity is through altering the balance between autoaggressive Th17 vs. protective Tregs.
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研究種目 : 基盤研究 (C) (一般)
研究期間 : 2016～2018
課題番号 : 16K08847
研究分野 : 分子生物学、免疫学
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