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Thrombo-Inflammation and Immunological Response in Ischemic Stroke: Focusing on Platelet-Tregs Interaction

Strokes are mainly caused by thromboembolic obstruction of a major cerebral artery. Major clinical manifestations include paralysis hemiplegia, aphasia, memory, and learning disorders. In the case of ischemic stroke (IS), hyperactive platelets contribute to advancing an acute thrombotic event progre...

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Autores principales: Cui, Jieqiong, Li, Huayan, Chen, Zongning, Dong, Ting, He, Xiying, Wei, Yuanyuan, Li, Zhengkun, Duan, Jinfeng, Cao, Ting, Chen, Qian, Ma, Dongmei, Zhou, Yang, Wang, Bo, Shi, Mingqin, Zhang, Qin, Xiong, Lei, Qin, Dongdong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9278516/
https://www.ncbi.nlm.nih.gov/pubmed/35846566
http://dx.doi.org/10.3389/fncel.2022.955385
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author Cui, Jieqiong
Li, Huayan
Chen, Zongning
Dong, Ting
He, Xiying
Wei, Yuanyuan
Li, Zhengkun
Duan, Jinfeng
Cao, Ting
Chen, Qian
Ma, Dongmei
Zhou, Yang
Wang, Bo
Shi, Mingqin
Zhang, Qin
Xiong, Lei
Qin, Dongdong
author_facet Cui, Jieqiong
Li, Huayan
Chen, Zongning
Dong, Ting
He, Xiying
Wei, Yuanyuan
Li, Zhengkun
Duan, Jinfeng
Cao, Ting
Chen, Qian
Ma, Dongmei
Zhou, Yang
Wang, Bo
Shi, Mingqin
Zhang, Qin
Xiong, Lei
Qin, Dongdong
author_sort Cui, Jieqiong
collection PubMed
description Strokes are mainly caused by thromboembolic obstruction of a major cerebral artery. Major clinical manifestations include paralysis hemiplegia, aphasia, memory, and learning disorders. In the case of ischemic stroke (IS), hyperactive platelets contribute to advancing an acute thrombotic event progression. Therefore, the principal goal of treatment is to recanalize the occluded vessel and restore cerebral blood flow by thrombolysis or mechanical thrombectomy. However, antiplatelets or thrombolytic therapy may increase the risk of bleeding. Beyond the involvement in thrombosis, platelets also contribute to the inflammatory process induced by cerebral ischemia. Platelet-mediated thrombosis and inflammation in IS lie primarily in the interaction of platelet receptors with endothelial cells and immune cells, including T-cells, monocytes/macrophages, and neutrophils. Following revascularization, intervention with conventional antiplatelet medicines such as aspirin or clopidogrel does not substantially diminish infarct development, most likely due to the limited effects on the thrombo-inflammation process. Emerging evidence has shown that T cells, especially regulatory T cells (Tregs), maintain immune homeostasis and suppress immune responses, playing a critical immunomodulatory role in ischemia-reperfusion injury. Hence, considering the deleterious effects of inflammatory and immune responses, there is an urgent need for more targeted agents to limit the thrombotic-inflammatory activity of platelets and minimize the risk of a cerebral hemorrhage. This review highlights the involvement of platelets in neuroinflammation and the evolving role of Tregs and platelets in IS. In response to all issues, preclinical and clinical strategies should generate more viable therapeutics for preventing and managing IS with immunotherapy targeting platelets and Tregs.
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spelling pubmed-92785162022-07-14 Thrombo-Inflammation and Immunological Response in Ischemic Stroke: Focusing on Platelet-Tregs Interaction Cui, Jieqiong Li, Huayan Chen, Zongning Dong, Ting He, Xiying Wei, Yuanyuan Li, Zhengkun Duan, Jinfeng Cao, Ting Chen, Qian Ma, Dongmei Zhou, Yang Wang, Bo Shi, Mingqin Zhang, Qin Xiong, Lei Qin, Dongdong Front Cell Neurosci Neuroscience Strokes are mainly caused by thromboembolic obstruction of a major cerebral artery. Major clinical manifestations include paralysis hemiplegia, aphasia, memory, and learning disorders. In the case of ischemic stroke (IS), hyperactive platelets contribute to advancing an acute thrombotic event progression. Therefore, the principal goal of treatment is to recanalize the occluded vessel and restore cerebral blood flow by thrombolysis or mechanical thrombectomy. However, antiplatelets or thrombolytic therapy may increase the risk of bleeding. Beyond the involvement in thrombosis, platelets also contribute to the inflammatory process induced by cerebral ischemia. Platelet-mediated thrombosis and inflammation in IS lie primarily in the interaction of platelet receptors with endothelial cells and immune cells, including T-cells, monocytes/macrophages, and neutrophils. Following revascularization, intervention with conventional antiplatelet medicines such as aspirin or clopidogrel does not substantially diminish infarct development, most likely due to the limited effects on the thrombo-inflammation process. Emerging evidence has shown that T cells, especially regulatory T cells (Tregs), maintain immune homeostasis and suppress immune responses, playing a critical immunomodulatory role in ischemia-reperfusion injury. Hence, considering the deleterious effects of inflammatory and immune responses, there is an urgent need for more targeted agents to limit the thrombotic-inflammatory activity of platelets and minimize the risk of a cerebral hemorrhage. This review highlights the involvement of platelets in neuroinflammation and the evolving role of Tregs and platelets in IS. In response to all issues, preclinical and clinical strategies should generate more viable therapeutics for preventing and managing IS with immunotherapy targeting platelets and Tregs. Frontiers Media S.A. 2022-06-29 /pmc/articles/PMC9278516/ /pubmed/35846566 http://dx.doi.org/10.3389/fncel.2022.955385 Text en Copyright © 2022 Cui, Li, Chen, Dong, He, Wei, Li, Duan, Cao, Chen, Ma, Zhou, Wang, Shi, Zhang, Xiong and Qin. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Cui, Jieqiong
Li, Huayan
Chen, Zongning
Dong, Ting
He, Xiying
Wei, Yuanyuan
Li, Zhengkun
Duan, Jinfeng
Cao, Ting
Chen, Qian
Ma, Dongmei
Zhou, Yang
Wang, Bo
Shi, Mingqin
Zhang, Qin
Xiong, Lei
Qin, Dongdong
Thrombo-Inflammation and Immunological Response in Ischemic Stroke: Focusing on Platelet-Tregs Interaction
title Thrombo-Inflammation and Immunological Response in Ischemic Stroke: Focusing on Platelet-Tregs Interaction
title_full Thrombo-Inflammation and Immunological Response in Ischemic Stroke: Focusing on Platelet-Tregs Interaction
title_fullStr Thrombo-Inflammation and Immunological Response in Ischemic Stroke: Focusing on Platelet-Tregs Interaction
title_full_unstemmed Thrombo-Inflammation and Immunological Response in Ischemic Stroke: Focusing on Platelet-Tregs Interaction
title_short Thrombo-Inflammation and Immunological Response in Ischemic Stroke: Focusing on Platelet-Tregs Interaction
title_sort thrombo-inflammation and immunological response in ischemic stroke: focusing on platelet-tregs interaction
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9278516/
https://www.ncbi.nlm.nih.gov/pubmed/35846566
http://dx.doi.org/10.3389/fncel.2022.955385
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