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血小板与白细胞在多发性硬化发病机制中的相互作用。

Interactions between platelets and leukocytes in pathogenesis of multiple sclerosis.

机构信息

Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Poland.

出版信息

Adv Clin Exp Med. 2019 Feb;28(2):277-285. doi: 10.17219/acem/83588.

DOI:10.17219/acem/83588
PMID:30411550
Abstract

Neurodegenerative diseases are an increasing problem in the modern world. Multiple sclerosis (MS) is a major human demyelinating and degenerative disease of the central nervous system (CNS). There are many reports that point to the significant role of platelet-leukocyte interaction in neurodegenerative diseases and cardiovascular disturbances. Epidemiological studies confirm the high risk of cardiovascular diseases in patients with MS. The pathophysiology mechanisms of this multi-component disease are very complex and involve various types of cells. There is increasing evidence that some co-stimulatory pathways affect the function of inflammatory cells, both in the periphery and in the CNS. Interactions of leukocytes and endothelial cells (ECs) could be significantly modulated in the presence of activated blood platelets. The supposed role of activated platelets in the development of vessel inflammatory response is due to their ability to adhere to inflamed ECs or proteins included in the subendothelial layer of the blood vessel wall, as well as to the ability of platelets to form aggregates with leukocytes. Blood platelets are able to directly activate leukocytes through a receptor-dependent mechanism or, indirectly, by biologically active compounds secreted from their granules. Cell-cell interactions provide critical mechanisms by which platelets link thrombosis, inflammation and related processes, such as diapedesis and leukocyte infiltration, to the affected vessel. Determining the relationship between platelet-leukocyte interactions and the development of neuroinflammation in the course of MS may provide new therapeutic targets in the future.

摘要

神经退行性疾病是现代社会日益严重的问题。多发性硬化症(MS)是一种主要的人类中枢神经系统(CNS)脱髓鞘和退行性疾病。有许多报道指出,血小板-白细胞相互作用在神经退行性疾病和心血管紊乱中起着重要作用。流行病学研究证实了 MS 患者患心血管疾病的高风险。这种多成分疾病的病理生理学机制非常复杂,涉及各种类型的细胞。越来越多的证据表明,一些共刺激途径会影响炎症细胞的功能,无论是在外周还是在中枢神经系统。白细胞和内皮细胞(ECs)之间的相互作用在活化的血小板存在下可以得到显著调节。活化的血小板在血管炎症反应发展中的假定作用归因于它们能够黏附在发炎的 ECs 或包含在血管壁的亚内皮层中的蛋白质上,以及血小板能够与白细胞形成聚集体的能力。血小板能够通过受体依赖性机制或通过从其颗粒中分泌的生物活性化合物间接直接激活白细胞。细胞-细胞相互作用提供了关键的机制,通过这些机制,血小板将血栓形成、炎症和相关过程(如血管外渗和白细胞浸润)与受影响的血管联系起来。确定血小板-白细胞相互作用与 MS 过程中神经炎症发展之间的关系,可能为未来提供新的治疗靶点。

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