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Interaction between ICAM1 in endothelial cells and LFA1 in T cells during the pathogenesis of experimental Parkinson's disease

Parkinson's disease (PD) is a chronic progressive disease that affects the central nervous system with a variety of symptoms. Although the precise etiology of PD is not yet fully understood, there is evidence to suggest that T cells serve an important role in the pathogenesis of PD. However, ho...

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Autores principales: Li, Wenjie, Chen, Sheng, Luo, Yuan, Xia, Yezi, Ma, Qianqian, Yao, Qi, Wu, Jianqing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388384/
https://www.ncbi.nlm.nih.gov/pubmed/32742344
http://dx.doi.org/10.3892/etm.2020.8758
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author Li, Wenjie
Chen, Sheng
Luo, Yuan
Xia, Yezi
Ma, Qianqian
Yao, Qi
Wu, Jianqing
author_facet Li, Wenjie
Chen, Sheng
Luo, Yuan
Xia, Yezi
Ma, Qianqian
Yao, Qi
Wu, Jianqing
author_sort Li, Wenjie
collection PubMed
description Parkinson's disease (PD) is a chronic progressive disease that affects the central nervous system with a variety of symptoms. Although the precise etiology of PD is not yet fully understood, there is evidence to suggest that T cells serve an important role in the pathogenesis of PD. However, how T cells are recruited in the brain tissue remains to be elucidated. The present study utilized human samples from patients with and without PD to investigate the infiltration of T cells in lesions in the central nervous system. A chemically-induced mouse PD model was also used to investigate the roles of T cells in the pathogenesis of PD. Depletion of CD4(+) or CD8(+) T cells was achieved using neutralizing antibodies. Adhesion molecule levels were assessed by flow cytometry. The results of the study indicated that T cell infiltration was evident in both human and murine samples of PD. Blocking CD4(+) or CD8(+) T cells attenuated the severity of murine PD. Intercellular adhesion molecule 1 (ICAM1 or CD54) was upregulated in mouse PD compared with controls, and its receptor, lymphocyte function-associated antigen-1 (LFA1) was overexpressed in T cells of the brain in PD mice compared with controls. Furthermore, inhibition of ICAM1 or LFA1 attenuated PD-associated characteristics in mice. In conclusion, the interaction between ICAM1 and LFA1 plays a role in recruiting T cells to the central nervous system to mediate experimental PD.
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spelling pubmed-73883842020-07-31 Interaction between ICAM1 in endothelial cells and LFA1 in T cells during the pathogenesis of experimental Parkinson's disease Li, Wenjie Chen, Sheng Luo, Yuan Xia, Yezi Ma, Qianqian Yao, Qi Wu, Jianqing Exp Ther Med Articles Parkinson's disease (PD) is a chronic progressive disease that affects the central nervous system with a variety of symptoms. Although the precise etiology of PD is not yet fully understood, there is evidence to suggest that T cells serve an important role in the pathogenesis of PD. However, how T cells are recruited in the brain tissue remains to be elucidated. The present study utilized human samples from patients with and without PD to investigate the infiltration of T cells in lesions in the central nervous system. A chemically-induced mouse PD model was also used to investigate the roles of T cells in the pathogenesis of PD. Depletion of CD4(+) or CD8(+) T cells was achieved using neutralizing antibodies. Adhesion molecule levels were assessed by flow cytometry. The results of the study indicated that T cell infiltration was evident in both human and murine samples of PD. Blocking CD4(+) or CD8(+) T cells attenuated the severity of murine PD. Intercellular adhesion molecule 1 (ICAM1 or CD54) was upregulated in mouse PD compared with controls, and its receptor, lymphocyte function-associated antigen-1 (LFA1) was overexpressed in T cells of the brain in PD mice compared with controls. Furthermore, inhibition of ICAM1 or LFA1 attenuated PD-associated characteristics in mice. In conclusion, the interaction between ICAM1 and LFA1 plays a role in recruiting T cells to the central nervous system to mediate experimental PD. D.A. Spandidos 2020-08 2020-05-15 /pmc/articles/PMC7388384/ /pubmed/32742344 http://dx.doi.org/10.3892/etm.2020.8758 Text en Copyright: © Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Li, Wenjie
Chen, Sheng
Luo, Yuan
Xia, Yezi
Ma, Qianqian
Yao, Qi
Wu, Jianqing
Interaction between ICAM1 in endothelial cells and LFA1 in T cells during the pathogenesis of experimental Parkinson's disease
title Interaction between ICAM1 in endothelial cells and LFA1 in T cells during the pathogenesis of experimental Parkinson's disease
title_full Interaction between ICAM1 in endothelial cells and LFA1 in T cells during the pathogenesis of experimental Parkinson's disease
title_fullStr Interaction between ICAM1 in endothelial cells and LFA1 in T cells during the pathogenesis of experimental Parkinson's disease
title_full_unstemmed Interaction between ICAM1 in endothelial cells and LFA1 in T cells during the pathogenesis of experimental Parkinson's disease
title_short Interaction between ICAM1 in endothelial cells and LFA1 in T cells during the pathogenesis of experimental Parkinson's disease
title_sort interaction between icam1 in endothelial cells and lfa1 in t cells during the pathogenesis of experimental parkinson's disease
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388384/
https://www.ncbi.nlm.nih.gov/pubmed/32742344
http://dx.doi.org/10.3892/etm.2020.8758
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