小鼠樹突狀細胞成熟前后的形態(tài)及其微絲蛋白的適應性改變
發(fā)布時間:2018-08-11 14:22
【摘要】: 目的研究樹突狀細胞(DC)成熟前后的形態(tài)及其微絲蛋白的適應性變化。 材料和方法經重組小鼠粒細胞-巨噬細胞集落刺激因子、白細胞介素-4誘導小鼠骨髓單核細胞為未成熟樹突狀細胞(imDC),培養(yǎng)至第6天時,用脂多糖(LPS)誘導成成熟樹突細胞(mDC),在倒置相差顯微鏡和熒光顯微鏡下觀察并前后對比分析細胞在成熟前后的表面突起和內部微絲蛋白(Filament Actin ,F-Actin)的變化。 結果 1. mDC高表達CD11c、MHC-Ⅱ和CD86。 2.成熟前的DC體積較小,隨著細胞的成熟,直徑逐漸增大,成熟過程中,DC表面突起逐漸增多、變粗且變長,呈怒張狀,在第7天達到高峰,以后突起逐漸松弛變軟,最后又回復至短細、稀疏狀態(tài)。 3.微絲蛋白主要集中于細胞膜和觸突上,其平均熒光強度在LPS刺激24 h后最高,48 h后明顯降低;細胞內F-肌動蛋白在成熟過程中逐漸減低,LPS刺激16 h后達高峰,以后細胞內又重新出現F-肌動蛋白的表達,且與細胞膜、突起間基本均勻一致。 結論 1.樹突狀細胞在成熟過程中體積逐漸增大,突起逐漸增多、增長,密度逐漸加大,其目的旨在盡可能地增大細胞的表面積,最大限度地發(fā)揮DC提取、呈遞抗原的功能。 2.細胞核逐漸增大,暗示細胞核在抗原的處理、加工過程中發(fā)揮著重要的作用;在此過程中,如微絲等細胞骨架也逐漸增生給予密切的配合。
[Abstract]:Objective to study the morphology of dendritic cells before and after (DC) maturation and the adaptive changes of microfilaments. Materials and methods Mouse bone marrow monocytes were induced to be immature dendritic cells (imDC),) cultured for 6 days by recombinant mouse granulocyte-macrophage colony stimulating factor (IL-4). The (mDC), of mature dendritic cells induced by lipopolysaccharide (LPS) was observed under inverted phase contrast microscope and fluorescence microscope, and the changes of (Filament Actin F-actin, a microfilament protein, were compared before and after maturation. Results 1. MDC overexpression of MHC- 鈪,
本文編號:2177247
[Abstract]:Objective to study the morphology of dendritic cells before and after (DC) maturation and the adaptive changes of microfilaments. Materials and methods Mouse bone marrow monocytes were induced to be immature dendritic cells (imDC),) cultured for 6 days by recombinant mouse granulocyte-macrophage colony stimulating factor (IL-4). The (mDC), of mature dendritic cells induced by lipopolysaccharide (LPS) was observed under inverted phase contrast microscope and fluorescence microscope, and the changes of (Filament Actin F-actin, a microfilament protein, were compared before and after maturation. Results 1. MDC overexpression of MHC- 鈪,
本文編號:2177247
本文鏈接:http://sikaile.net/yixuelunwen/shiyanyixue/2177247.html
最近更新
教材專著