Neutrophils and viral-induced neurologic disease.

Neutrophils and viral-induced neurologic disease.
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DOI:
10.1016/j.clim.2016.05.009
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发表时间:
2018-04
期刊:
Clinical immunology (Orlando, Fla.)
影响因子:
--
通讯作者:
Lane TE
Lane TE
中科院分区:
其他
文献类型:
--
作者:
Grist JJ;Marro B;Lane TE

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嗜神经性病毒对中枢神经系统(CNS)的感染代表了在所有年龄的人的发病率和死亡率方面日益增加的世界性问题。虽然血脑屏障(BBB)的独特结构特征提供了物理和生理屏障,但许多嗜神经病毒能够进入CNS,导致各种病理结果。尽管如此,抗原特异性淋巴细胞最终能够在CNS内积累,并通过减少或消除入侵的病毒病原体来促进防御。或者,免疫系统的活化细胞的浸润可能是有害的,因为这些细胞可能导致可能导致长期细胞损伤或死亡的神经病理学。最近,髓样细胞例如嗜中性粒细胞已经涉及响应于CNS的病毒感染而促进宿主防御和疾病。这篇综述强调了最近的研究,使用冠状病毒诱导的神经系统疾病作为模型,以确定中性粒细胞如何影响病毒复制以及脱髓鞘的有效控制。嗜神经病毒感染后,中性粒细胞迅速从骨髓动员到中枢神经系统。嗜中性粒细胞通过与嗜中性粒细胞表面表达的受体CXCR2结合来响应趋化因子配体,包括CXCL 1和CXCL 2。嗜中性粒细胞对宿主防御的贡献包括增加血脑屏障的通透性以允许病毒特异性淋巴细胞进入。嗜中性粒细胞还可增加神经病理学的严重性,例如脱髓鞘,如通过使用转基因小鼠模型系统所证明的。
Infection of the central nervous system (CNS) by neurotropic viruses represents an increasing worldwide problem in terms of morbidity and mortality for people of all ages. Although unique structural features of the blood-brain-barrier (BBB) provide a physical and physiological barrier, a number of neurotropic viruses are able to enter the CNS resulting in a variety of pathological outcomes. Nonetheless, antigen-specific lymphocytes are ultimately able to accumulate within the CNS and contribute to defense by reducing or eliminating the invading viral pathogen. Alternatively, infiltration of activated cells of the immune system may be detrimental, as these cells can contribute to neuropathology that may result in long-term cellular damage or death. More recently, myeloid cells e.g. neutrophils have been implicated in contributing to both host defense and disease in response to viral infection of the CNS. This review highlights recent studies using coronavirus-induced neurologic disease as a model to determine how neutrophils affect effective control of viral replication as well as demyelination. Neutrophils are rapidly mobilized from the bone-marrow to the central nervous system following infection with neurotropic viruses. Neutrophils respond to chemokine ligands including CXCL1 and CXCL2 by binding to the receptor CXCR2 expressed upon the neutrophil cell surface. Contributions to host defense by neutrophils include increasing the permeability of the blood-brain-barrier to allow access by virus-specific lymphocytes. Neutrophils can also increase the severity of neuropathology e.g. demyelination as evidenced through use of transgenic mouse model systems.
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