单核细胞
血小板因子4
趋化因子
细胞生物学
生物
肿瘤坏死因子α
癌症研究
免疫学
血小板
化学
炎症
作者
Barbara Scheuerer,Martin Ernst,Iris Dürrbaum-Landmann,Jens Fleischer,Evelin Grage-Griebenow,Ernst Brandt,Hans‐Dieter Flad,Frank Petersen
出处
期刊:Blood
[American Society of Hematology]
日期:2000-02-15
卷期号:95 (4): 1158-1166
被引量:280
标识
DOI:10.1182/blood.v95.4.1158.004k31_1158_1166
摘要
Unstimulated monocytes rapidly undergo physiological changes resulting in programmed cell death (apoptosis) while stimuli promoting differentiation of these cells into macrophages were shown to inhibit apoptotic processes. In the present study, we report that the platelet-derived -chemokine platelet factor 4 (PF4) induces the differentiation of monocytes into macrophages, as is evident from morphological changes as well as from the up-regulation of differentiation markers (carboxypeptidase M/MAX1 and CD71). Significant alterations of the phenotype were observed after 72 hours of culture in the presence of the chemokine and required a minimal concentration of 625 nmol/L PF4. PF4-induced macrophages were characterized by a lack of HLA-DR antigen on their surface but showed a strong increase in the expression of the CD28 ligand B7-2. Furthermore, PF4 stimulation prevented monocytes from undergoing spontaneous apoptosis during 72 hours of culture as determined in an annexin-V–binding assay. Although PF4 induced the secretion of relevant amounts of TNF-, neutralizing antibodies directed against TNF- or granulocyte-macrophage colony–stimulating factor (GM-CSF) did not revert PF4-induced rescue from programmed cell death, suggesting that PF4 exerts its antiapoptotic effects in a TNF-– or GM-CSF–independent fashion. On the basis of these results, we propose a novel role for PF4 in the control of monocyte differentiation during an inflammatory process in vivo.
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