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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Main Authors: David R. Beers, Weihua Zhao, Jason R. Thonhoff, Alireza Faridar, Aaron D. Thome, Shixiang Wen, Jinghong Wang, Stanley H. Appel
Format: Article
Language:English
Published: Elsevier 2021-03-01
Series:Brain, Behavior, & Immunity - Health
Subjects:
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.
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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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