Cargando…
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...
Autores principales: | , , , , , , |
---|---|
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 |
_version_ | 1783564297923723264 |
---|---|
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. |
format | Online Article Text |
id | pubmed-7388384 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT liwenjie interactionbetweenicam1inendothelialcellsandlfa1intcellsduringthepathogenesisofexperimentalparkinsonsdisease AT chensheng interactionbetweenicam1inendothelialcellsandlfa1intcellsduringthepathogenesisofexperimentalparkinsonsdisease AT luoyuan interactionbetweenicam1inendothelialcellsandlfa1intcellsduringthepathogenesisofexperimentalparkinsonsdisease AT xiayezi interactionbetweenicam1inendothelialcellsandlfa1intcellsduringthepathogenesisofexperimentalparkinsonsdisease AT maqianqian interactionbetweenicam1inendothelialcellsandlfa1intcellsduringthepathogenesisofexperimentalparkinsonsdisease AT yaoqi interactionbetweenicam1inendothelialcellsandlfa1intcellsduringthepathogenesisofexperimentalparkinsonsdisease AT wujianqing interactionbetweenicam1inendothelialcellsandlfa1intcellsduringthepathogenesisofexperimentalparkinsonsdisease |