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J-GLOBAL ID：201802271155802254   整理番号：18A0279951

脂肪由来幹細胞は2型糖尿病ApoE~ / マウスにおけるCD4~+T細胞の増殖及び分極化を制限における障害【Powered by NICT】

Adipose-derived stem cells were impaired in restricting CD4⁺T cell proliferation and polarization in type 2 diabetic ApoE^-/- mouse

著者 (15件)： Liu Ming-hao (The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong ...) ,  Li Ya (The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong ...) ,  Han Lu (The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong ...) ,  Han Lu (Department of General Practice, Qilu Hospital of Shandong University, Ji’nan, China) ,  Zhang Yao-yuan (The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong ...) ,  Wang Di (The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong ...) ,  Wang Zhi-hao (The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong ...) ,  Wang Zhi-hao (Department of Geriatrics, Qilu Hospital of Shandong University, Ji’nan, China) ,  Zhou Hui-min (The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong ...) ,  Song Ming (The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong ...) ,  Li Yi-hui (The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong ...) ,  Tang Meng-xiong (The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong ...) ,  Tang Meng-xiong (Department of Emergency, Qilu Hospital of Shandong University, Ji’nan, China) ,  Zhang Wei (The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong ...) ,  Zhong Ming (The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong ...)
資料名： Molecular Immunology  (Molecular Immunology)
巻： 87  ページ： 152-160  発行年： 2017年 
JST資料番号： B0850A  ISSN： 0161-5890  CODEN： IMCHAZ  資料種別： 逐次刊行物 (A)
記事区分： 原著論文  発行国： オランダ (NLD)  言語： 英語 (EN)

抄録/ポイント： アテローム性動脈硬化症(AS)は,2型糖尿病(T2DM)の最も一般的で重篤な合併症であり,慢性全身性炎症よりむしろ高血糖により加速される。脂肪組織は異常な代謝状態における全身性炎症の主要な源である。炎症性CD4~+T細胞は脂肪炎症の促進において重要な役割を果たす。脂肪再生のための脂肪組織由来幹細胞(ADSC)は,免疫抑制の強力な能力を持ち,CD4~+T細胞を制限する。T2DM ADSCである拮抗CD4~+T細胞増殖と分極の障害かどうか不明のままである。は2型糖尿病ApoE~ / マウスモデルを構築し,in vivoで間質-血管画分(SVF)におけるCD4~+T細胞の浸潤と部分群を試験した。CD4選別なしNormal/T2DM ADSCと正常ひ細胞はex vivoで異なるスケールでの分離と共培養した。ADSCのプロ及び抗炎症の免疫表現型も調べた。フローサイトメトリー(FCM)及びELISAは,上記実験に適用した。CD4~+T細胞はin vivoでT2DM ApoE~ / マウスの脂肪組織における炎症性表現型を行った。CD4~+T細胞増殖と偏光に制限はex vivo T2DM ADSCと共培養した後に明らかに弱い明らかにされた。著明な差異は両ADSCの形態と成長型では見られなかった。しかし,T2DM ADSCは炎症性免疫表現型を獲得し,より少ないPGE_2を分泌し,高いMHC-IIと共刺激分子(CD40, CD80)を発現する。T2DM SVF上清で培養した後の正常ADSCも表現型変化を得ることができた。2型糖尿病ApoE~ / マウスにおける脂肪組織に存在するCD4~+T細胞浸潤と炎症誘発性分極。T2DM ADSCは免疫表現型変化によるCD4~+Tリンパ球増殖および炎症誘発性分極を制限する機能障害を有していた。Copyright 2018 Elsevier B.V., Amsterdam. All rights reserved. Translated from English into Japanese by JST.【Powered by NICT】

シソーラス用語： *CD4抗原 ,  消炎作用 ,  脂肪組織 ,  機能障害 ,  表現型 ,  アテローム性動脈硬化症 ,  細胞増殖 ,  炎症 ,  フローサイトメトリー ,  血管 ,  免疫抑制 ,  *2型糖尿病 ,  *分極 ,  ELISA ,  共培養

著者キーワード (5件)： 脂肪炎症 ,  脂肪由来幹細胞 ,  CD4~+T細胞 ,  Proliferation ,  炎症誘発性分極

分類 (1件)： 細胞生理一般  (EF02010S)

タイトルに関連する用語 (7件)： 脂肪由来幹細胞 ,  2型糖尿病 ,  マウス ,  増殖 ,  分極 ,  制限 ,  障害