Induction of CD69 activation molecule on human neutrophils by GM-CSF, IFN-γ, and IFN-α
Induction of CD69 activation molecule on human neutrophils by GM-CSF, IFN-γ, and IFN-α
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DOI：
10.1016/s0008-8749(03)00002-9
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发表时间：
2002-11-01
影响因子：
4.3
通讯作者：
Capsoni, F
中科院分区：
文献类型：
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作者：
Atzeni, F;Schena, M;Capsoni, F
CD 69糖蛋白是T和B淋巴细胞的早期活化抗原，但其表达在大多数造血谱系的细胞（包括用PMA或fMLP刺激后的嗜中性粒细胞）上被体外诱导。在这项研究中，我们研究了人类中性粒细胞上的CD 69表达是否可以通过炎症或抗炎细胞因子（IL-1 β、IL-2、IL-4、IL-6、IL-8、IL-10、IL-12、IL-18、G-CSF、GM-CSF、TNF-α、TGF-β、IFN-α、IFN-γ）调节。来自健康受试者的静息中性粒细胞在细胞表面上不表达CD 69;此外，在这些细胞中不明显存在预先形成的CD 69细胞内池。在培养基中过夜孵育后，在这些细胞上几乎检测不到CD 69，而与GM-CSF、IFN-γ或IFN-α过夜孵育显著诱导中性粒细胞上的CD 69表达，其中GM-CSF似乎是最有效的诱导剂。这种诱导依赖于新的蛋白质合成，因为它被放线菌酮显著抑制（约50%抑制）。GM-CSF致敏的中性粒细胞上的CD 69交联与LPS发生反应，并增加TNF-α的产生和分泌，这表明CD 69阳性中性粒细胞在不同炎症性疾病的发病机制和维持中发挥作用。(C)2003 Elsevier Science（美国）。All rights reserved.
The CD69 glycoprotein is an early activation antigen of T and B lymphocytes but it expression is induced in vitro on cells of most hematopoietic lineages, including neutrophils after stimulation with PMA or fMLP. In this study, we investigated whether CD69 expression on human neutrophils could be modulated by inflammatory or anti-inflammatory cytokines (IL-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-18, G-CSF, GM-CSF, TNF-alpha,TGF-beta, IFN-alpha, IFN-gamma). Resting neutrophils from healthy subjects did not express CD69 on the cell surface; moreover, a preformed intracellular pool of CD69 was not evident in these cells. CD69 was barely detectable on these cells after overnight incubation in medium while overnight incubation with GM-CSF, IFN-gamma or IFN-alpha significantly induced CD69 expression on neutrophils with GM-CSF appearing to be the most potent inducer. This induction was dependent on a new protein synthesis as it was significantly inhibited by cycloheximide (about 50% inhibition). CD69 cross-linking on GM-CSF-primed neutrophils sinergized with LPS and increased TNF-alpha production and secretion suggesting a role for CD69-positive neutrophils in the pathogenesis and maintenance of different inflammatory diseases. (C) 2003 Elsevier Science (USA). All rights reserved.