The β-thromboglobulins and platelet factor 4:: blood platelet-derived CXC chemokines with divergent roles in early neutrophil regulation
The β-thromboglobulins and platelet factor 4:: blood platelet-derived CXC chemokines with divergent roles in early neutrophil regulation
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DOI：
10.1002/jlb.67.4.471
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发表时间：
2000-04-01
影响因子：
5.5
通讯作者：
Flad, HD
中科院分区：
文献类型：
--
作者：
Brandt, E;Petersen, F;Flad, HD
中性粒细胞向组织损伤部位的募集是宿主防御过程中最早的事件之一。属于趋化因子CXC亚家族的几种趋化性细胞因子被认为与这种反应有关。特别是那些储存在血小板中并在激活后立即释放的CXC趋化因子可能在炎症发作时主导嗜中性粒细胞依赖性宿主防御。主要的血小板衍生的CXC趋化因子是β-血小板球蛋白和血小板因子4（PF-4），它们都以微摩尔浓度释放到血液中。这些介质的可用性以及功能活动似乎受到各种监管机制的严格控制。这些包括趋化因子前体的蛋白水解加工、寡聚体形成和嗜中性粒细胞表达受体的差异使用。在此，我们回顾了我们的工作，早期中性粒细胞调节PF-4，β-血小板球蛋白嗜中性粒细胞激活肽2（NAP-2）及其主要前体结缔组织激活肽III（CTAP-III）。此外，我们提出了一个模型来评估这些趋化因子的贡献，以协调招聘和激活的中性粒细胞在急性组织损伤。
The recruitment of neutrophil granulocytes to sites of tissue injury is one of the earliest events during host defense. Several chemotactic cytokines belonging to the CXC subfamily of chemokines are thought to be implicated in this kind of response. Especially those CXC chemokines that are stored in blood platelets and become immediately released upon activation are likely to dominate neutrophil-dependent host defense at the onset of inflammation. The major platelet-derived CXC chemokines are the beta-thromboglobulins and platelet factor 4 (PF-4), which are both released into the blood at micromolar concentrations. The availability as well as the functional activity of these mediators appear to be subject to tight control by diverse regulatory mechanisms. These include proteolytic processing of chemokine precursors, oligomer formation, and the differential usage of neutrophil-expressed receptors. Herein we review our work on early neutrophil regulation by PF-4, the beta-thromboglobulin neutrophil-activating peptide 2 (NAP-2) and its major precursor connective tissue-activating peptide III (CTAP-III). We moreover propose a model to assess the contribution by either of these chemokines to coordinated recruitment and activation of neutrophils in response to acute tissue injury.