Expression Data from murine control and IL6ralpha-deficient macrophages stimulated with Interleukin-6. Mus musculus

IL-6 induces IL4ralpha expression in macrophages. This mechanism is necessary to promote macrophage polarization towards an M2-phenotype and is crucial to limit the inflammatory response both upon obesity and LPS-endotoxemia. In this dataset, we include the expression data obtained from primary murine bone marrow-derived macrophages from control and IL6ralpha-deficient macrophages (n=4vs4) stimulated with interleukin-6 (IL-6) Overall design: 8 samples were analyzed to compare control and IL6ralpha-deficient macrophages for their gene expression profiles upon stimulation with IL-6

白细胞介素6（IL-6）可诱导巨噬细胞（macrophages）中白细胞介素4受体α链（IL4ralpha）的表达。该机制是促进巨噬细胞向M2表型极化的必要条件，同时在肥胖与脂多糖内毒素血症（LPS-endotoxemia）两种情境下，对限制炎症反应均至关重要。
本数据集包含经白细胞介素6（IL-6）刺激的对照组与IL6ralpha缺陷型原代小鼠骨髓源性巨噬细胞（primary murine bone marrow-derived macrophages）的表达谱数据，两组样本量均为4（n=4 vs 4）。
实验设计概述：本研究共分析8份样本，用于对比经IL-6刺激后，对照组与IL6ralpha缺陷型巨噬细胞的基因表达谱（gene expression profiles）差异。