摘要
目的:探索IL-34与M-CSF在诱导骨髓细胞向巨噬细胞分化以及巨噬细胞表型维持中的异质性作用。方法:小鼠骨髓细胞经不同方案培养后,观察细胞形态并计数;流式分析巨噬细胞比例、分化标记物表达水平和细胞凋亡水平;RT-PCR检测巨噬细胞极化相关基因的表达水平。结果:与M-CSF比较,IL-34诱导巨噬细胞在形态、比例和绝对数差异均无显著统计学意义;分化标记物CD11b和F4/80的平均荧光强度(MFI)显著降低(均P<0.05);极化相关基因IL-1β、IL-10和iNOS的表达水平显著升高(均P<0.05),IL-12β表达降低(均P<0.05)。结论:IL-34可诱导骨髓细胞向巨噬细胞分化,促进巨噬细胞增殖的能力与M-CSF相似;促进巨噬细胞分化相关标记和极化相关基因表达与M-CSF存在显著差异。
Objective: To explore the different effect of IL-34 and M-CSF in induction of bone marrow cells differentiation into macrophages and maintenance of macrophage phenotype. Methods: Bone marrow cells were cultured with different cytokines.The number of macrophages was counted and their morphology was observed under microscope.The proportion of macrophages,expression of differentiation markers and apoptosis were determined by flow cytometry.The expression of polarization-related genes in macrophages was detected by RT-PCR. Results: Compared with the M-CSF group,there was no significant difference in morphology,proportion and absolute number of macrophages in IL-34 group.Mean fluorescence intensity (MFI) of the differentiation markers CD11b and F4/80 was significantly reduced ( P <0.05).The expression of polarization-related genes IL- 1β, IL-10 and iNOS was significantly increased ( P <0.05), while the expression of IL- 12 β was decreased ( P <0.05). Conclusion: IL-34 shares similar effect with M-CSF in induction of differentiation and proliferation of macrophages from bone marrow cells.But IL-34 is different from M-CSF in the expression of differentiation markers and polarization-related genes in macrophages.
作者
刘晓礼
王昊
张东玥
王丽娜
郑国光
LIU Xiao-Li;WANG Hao;ZHANG Dong-Yue;WANG Li-Na;ZHENG Guo-Guang(State Key Laboratory of Experimental Hematology,National Clinical Research Center for Blood Diseases,Institute of Hematology & Blood Diseases Hospital,Chinese Academy of Medical Sciences & Peking Union Medical College,Tianjin 300020,China)
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2019年第14期1671-1676,共6页
Chinese Journal of Immunology
基金
国家自然科学基金(No.81570153,No.81770183)
中国医学科学院医学与健康科技工程创新医学项目基金(No.2016-I2M-2-006,No.2017-I2M-1-015)
天津自然科学基金(No.17JCZDJC35000)资助