THEINNATE IMMUNITY CELLS IN THE PATHOGENESIS OF TRAUMATIC BRAIN INJURY
- 作者: Radkov I.1, Plekhova N.1, Zinoviev S.1, Shumatov V.1
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隶属关系:
- Pacific State Medical University
- 期: 卷 22, 编号 2-1 (2019)
- 页面: 480-481
- 栏目: ORIGINAL ARTICLES
- URL: https://journals.rcsi.science/1028-7221/article/view/120273
- DOI: https://doi.org/10.31857/S102872210006937-5
- ID: 120273
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详细
The content of innate immunity cells expressing CD45, CD14, CD16, CD11b and F4 / 80 receptors brain in experimental modeling of traumatic brain injury (TBI) was studed. It was established that the number of CD16/11b positive macrophages of the M1 subpopulation increased in microgy on the 2nd day after TBI and signifi cantly enlarged up to 8 days. In the corpus callosum and the ipsilateral area of the striatum, CD16/11b expressed cells also peaked 8 days after TBI and correlated with an increase in the positive response to the presence of the endothelial antigen SMI71. Signifi cant structural transformations of the nervous tissue and the output of peripheral immune cells, coupled with impaired permeability by the blood-brain barrier, were shown. The disturbance of regulatory changes neuroimmune connections in TBI was proved.
作者简介
I. Radkov
Pacific State Medical University
编辑信件的主要联系方式.
Email: fake@neicon.ru
Post-Graduate Student, Central Research Laboratory,
Vladivostok
俄罗斯联邦N. Plekhova
Pacific State Medical University
Email: pl_nat@hotmail.com
Dr, Head of the Central Research Laboratory,
Vladivostok
俄罗斯联邦S. Zinoviev
Pacific State Medical University
Email: fake@neicon.ru
PhD, Senior Researcher, Central Research Laboratory,
Vladivostok
俄罗斯联邦V. Shumatov
Pacific State Medical University
Email: fake@neicon.ru
Dr, professor, rector,
Vladivostok
俄罗斯联邦参考
- Hellewell S. C., Morganti-Kossmann M. C. Guilty molecules, guilty minds? The conflicting roles of the innate immune response to traumatic brain injury. Mediators Inflamm. 2012, 2012: 356494.
- Pop V., Sorensen D. W., Kamper J. E., Ajao D. O., Murphy M. P., Head E., Hartman R. E., Badaut J. Early brain injury alters the blood-brain barrier phenotype in parallel with β-amyloid and cognitive changes in adulthood // J Cereb Blood Flow Metab. 2013 Feb; 33(2): 205–14