Serum programmed cell death proteins in amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis (ALS) is a multifactorial, multisystem pro-inflammatory neuromuscular disorder. Activation of programmed cell death-1 (PD-1), and its ligands, programmed cell death-ligand 1 and 2 (PD-L1/L2), leads to immune suppression. Serum soluble forms of these proteins, sPD-1/sPD-...
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Format: | Article |
Language: | English |
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Elsevier
2021-03-01
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Series: | Brain, Behavior, & Immunity - Health |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S2666354621000120 |
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author | David R. Beers Weihua Zhao Jason R. Thonhoff Alireza Faridar Aaron D. Thome Shixiang Wen Jinghong Wang Stanley H. Appel |
author_facet | David R. Beers Weihua Zhao Jason R. Thonhoff Alireza Faridar Aaron D. Thome Shixiang Wen Jinghong Wang Stanley H. Appel |
author_sort | David R. Beers |
collection | DOAJ |
description | Amyotrophic lateral sclerosis (ALS) is a multifactorial, multisystem pro-inflammatory neuromuscular disorder. Activation of programmed cell death-1 (PD-1), and its ligands, programmed cell death-ligand 1 and 2 (PD-L1/L2), leads to immune suppression. Serum soluble forms of these proteins, sPD-1/sPD-L1/sPD-L2, inhibit this suppression and promote pro-inflammatory responses. The purpose of this study was to determine if sPD-1, sPD-L1, and sPD-L2 were increased in sera of patients with ALS. sPD-1 and sPD-L2 were elevated in sera of patients and accurately reflected patients’ disease burdens. Increased sera levels of programmed cell death proteins reinforce the concept that peripheral pro-inflammatory responses contribute to systemic inflammation in patients with ALS. |
first_indexed | 2024-12-18T01:49:58Z |
format | Article |
id | doaj.art-02c2c05243564fc2af7fc3db2353d077 |
institution | Directory Open Access Journal |
issn | 2666-3546 |
language | English |
last_indexed | 2024-12-18T01:49:58Z |
publishDate | 2021-03-01 |
publisher | Elsevier |
record_format | Article |
series | Brain, Behavior, & Immunity - Health |
spelling | doaj.art-02c2c05243564fc2af7fc3db2353d0772022-12-21T21:25:05ZengElsevierBrain, Behavior, & Immunity - Health2666-35462021-03-0112100209Serum programmed cell death proteins in amyotrophic lateral sclerosisDavid R. Beers0Weihua Zhao1Jason R. Thonhoff2Alireza Faridar3Aaron D. Thome4Shixiang Wen5Jinghong Wang6Stanley H. Appel7Peggy and Gary Edwards ALS Laboratory, Department of Neurology, Houston Methodist Neurological Institute, Houston Methodist Research Institute, Houston Methodist Hospital, Houston, TX, USAPeggy and Gary Edwards ALS Laboratory, Department of Neurology, Houston Methodist Neurological Institute, Houston Methodist Research Institute, Houston Methodist Hospital, Houston, TX, USAPeggy and Gary Edwards ALS Laboratory, Department of Neurology, Houston Methodist Neurological Institute, Houston Methodist Research Institute, Houston Methodist Hospital, Houston, TX, USAPeggy and Gary Edwards ALS Laboratory, Department of Neurology, Houston Methodist Neurological Institute, Houston Methodist Research Institute, Houston Methodist Hospital, Houston, TX, USAPeggy and Gary Edwards ALS Laboratory, Department of Neurology, Houston Methodist Neurological Institute, Houston Methodist Research Institute, Houston Methodist Hospital, Houston, TX, USAPeggy and Gary Edwards ALS Laboratory, Department of Neurology, Houston Methodist Neurological Institute, Houston Methodist Research Institute, Houston Methodist Hospital, Houston, TX, USAPeggy and Gary Edwards ALS Laboratory, Department of Neurology, Houston Methodist Neurological Institute, Houston Methodist Research Institute, Houston Methodist Hospital, Houston, TX, USACorresponding author. Department of Neurology, Houston Methodist Neurological Institute, 6560 Fannin Street, Suite ST-802, Houston, TX, 77030, USA.; Peggy and Gary Edwards ALS Laboratory, Department of Neurology, Houston Methodist Neurological Institute, Houston Methodist Research Institute, Houston Methodist Hospital, Houston, TX, USAAmyotrophic lateral sclerosis (ALS) is a multifactorial, multisystem pro-inflammatory neuromuscular disorder. Activation of programmed cell death-1 (PD-1), and its ligands, programmed cell death-ligand 1 and 2 (PD-L1/L2), leads to immune suppression. Serum soluble forms of these proteins, sPD-1/sPD-L1/sPD-L2, inhibit this suppression and promote pro-inflammatory responses. The purpose of this study was to determine if sPD-1, sPD-L1, and sPD-L2 were increased in sera of patients with ALS. sPD-1 and sPD-L2 were elevated in sera of patients and accurately reflected patients’ disease burdens. Increased sera levels of programmed cell death proteins reinforce the concept that peripheral pro-inflammatory responses contribute to systemic inflammation in patients with ALS.http://www.sciencedirect.com/science/article/pii/S2666354621000120Amyotrophic lateral sclerosisNeuromuscular diseaseNeurodegenerationProgram cell death proteinsInflammationImmune regulatory checkpoint pathways |
spellingShingle | David R. Beers Weihua Zhao Jason R. Thonhoff Alireza Faridar Aaron D. Thome Shixiang Wen Jinghong Wang Stanley H. Appel Serum programmed cell death proteins in amyotrophic lateral sclerosis Brain, Behavior, & Immunity - Health Amyotrophic lateral sclerosis Neuromuscular disease Neurodegeneration Program cell death proteins Inflammation Immune regulatory checkpoint pathways |
title | Serum programmed cell death proteins in amyotrophic lateral sclerosis |
title_full | Serum programmed cell death proteins in amyotrophic lateral sclerosis |
title_fullStr | Serum programmed cell death proteins in amyotrophic lateral sclerosis |
title_full_unstemmed | Serum programmed cell death proteins in amyotrophic lateral sclerosis |
title_short | Serum programmed cell death proteins in amyotrophic lateral sclerosis |
title_sort | serum programmed cell death proteins in amyotrophic lateral sclerosis |
topic | Amyotrophic lateral sclerosis Neuromuscular disease Neurodegeneration Program cell death proteins Inflammation Immune regulatory checkpoint pathways |
url | http://www.sciencedirect.com/science/article/pii/S2666354621000120 |
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