Mannose-binding Lectin Mediated Complement Pathway in Autoimmune Neurological Disorders
Multiple sclerosis (MS) is a complex, demyelinating disease of the central nervous system (CNS) with variable phenotypic presentations, while Guillain-Barre Syndrome (GBS) is the prototypic acute inflammatory disorder that affects the peripheral nervous system. Myasthenia gravis (MG) is a T cell de...
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Tehran University of Medical Sciences
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doaj-d2ae6bdea92b41e8bf9691212d8b30da2020-11-25T04:12:40ZengTehran University of Medical SciencesIranian Journal of Allergy, Asthma and Immunology1735-15021735-52492016-06-01153604Mannose-binding Lectin Mediated Complement Pathway in Autoimmune Neurological DisordersMehrdad Farrokhi0Mehrnoosh Dabirzadeh1Nastaran Dastravan2Masoud Etemadifar3Keyvan Ghadimi4Zahra Saadatpour5Ali Rezaei6Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, IranDepartment of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, IranDepartment of Biology, Faculty of Sciences, University of Isfahan, Isfahan, IranMultiple Sclerosis and Neuroimmunology Research Center, Isfahan, IranDepartment of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, IranDepartment of Radiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, IranDepartment of Radiology, School of Medicine, Najafabad Branch, Islamic Azad University, Isfahan, Iran Multiple sclerosis (MS) is a complex, demyelinating disease of the central nervous system (CNS) with variable phenotypic presentations, while Guillain-Barre Syndrome (GBS) is the prototypic acute inflammatory disorder that affects the peripheral nervous system. Myasthenia gravis (MG) is a T cell dependent and antibody mediated autoimmune disease. Although it has been shown that complement plays a critical role in the pathogenesis of MS, GBS, and MG, the role of mannose-binding lectin (MBL) as a biomarker of immunopathogensis of these diseases and also its association with the severity of them have been poorly investigated. Therefore, in this study we aimed to measure plasma levels of MBL in patients with MS, GBS, and MG. In a case-control study, plasma was obtained from healthy controls (n=100) and also patients with MS (n=120), GBS (n=30), and MG (n=30). Plasma level measurement of MBL was performed using enzyme-linked immunosorbent assay (ELISA). The mean serum level of MBL was significantly different between groups of patients and healthy controls (p<0.001). We also found a positive correlation between plasma levels of MBL and severity scores of MS, MG, and GBS patients including: expanded disability status scale (EDSS) (r=+0.60 and p=<0.001), quantitative myasthenia gravis score (QMGS) (r=+0.56 and p=0.01), and GBS disability scale (GDS) (r=+0.37 and p=0.04). Taken together, our findings suggest that complement activation mediated by MBL contributes to the pathogenesis and also severity of MS, MG, and GBS. However, because the lectin pathway can be involved in several phases of the immune response, further evidence will be required to elucidate the underlying mechanism. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/645AutoimmunityComplement system proteinsGuillain-Barre syndromeMannose-binding lectinMultiple sclerosisMyasthenia gravis |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Mehrdad Farrokhi Mehrnoosh Dabirzadeh Nastaran Dastravan Masoud Etemadifar Keyvan Ghadimi Zahra Saadatpour Ali Rezaei |
spellingShingle |
Mehrdad Farrokhi Mehrnoosh Dabirzadeh Nastaran Dastravan Masoud Etemadifar Keyvan Ghadimi Zahra Saadatpour Ali Rezaei Mannose-binding Lectin Mediated Complement Pathway in Autoimmune Neurological Disorders Iranian Journal of Allergy, Asthma and Immunology Autoimmunity Complement system proteins Guillain-Barre syndrome Mannose-binding lectin Multiple sclerosis Myasthenia gravis |
author_facet |
Mehrdad Farrokhi Mehrnoosh Dabirzadeh Nastaran Dastravan Masoud Etemadifar Keyvan Ghadimi Zahra Saadatpour Ali Rezaei |
author_sort |
Mehrdad Farrokhi |
title |
Mannose-binding Lectin Mediated Complement Pathway in Autoimmune Neurological Disorders |
title_short |
Mannose-binding Lectin Mediated Complement Pathway in Autoimmune Neurological Disorders |
title_full |
Mannose-binding Lectin Mediated Complement Pathway in Autoimmune Neurological Disorders |
title_fullStr |
Mannose-binding Lectin Mediated Complement Pathway in Autoimmune Neurological Disorders |
title_full_unstemmed |
Mannose-binding Lectin Mediated Complement Pathway in Autoimmune Neurological Disorders |
title_sort |
mannose-binding lectin mediated complement pathway in autoimmune neurological disorders |
publisher |
Tehran University of Medical Sciences |
series |
Iranian Journal of Allergy, Asthma and Immunology |
issn |
1735-1502 1735-5249 |
publishDate |
2016-06-01 |
description |
Multiple sclerosis (MS) is a complex, demyelinating disease of the central nervous system (CNS) with variable phenotypic presentations, while Guillain-Barre Syndrome (GBS) is the prototypic acute inflammatory disorder that affects the peripheral nervous system. Myasthenia gravis (MG) is a T cell dependent and antibody mediated autoimmune disease. Although it has been shown that complement plays a critical role in the pathogenesis of MS, GBS, and MG, the role of mannose-binding lectin (MBL) as a biomarker of immunopathogensis of these diseases and also its association with the severity of them have been poorly investigated. Therefore, in this study we aimed to measure plasma levels of MBL in patients with MS, GBS, and MG. In a case-control study, plasma was obtained from healthy controls (n=100) and also patients with MS (n=120), GBS (n=30), and MG (n=30). Plasma level measurement of MBL was performed using enzyme-linked immunosorbent assay (ELISA). The mean serum level of MBL was significantly different between groups of patients and healthy controls (p<0.001). We also found a positive correlation between plasma levels of MBL and severity scores of MS, MG, and GBS patients including: expanded disability status scale (EDSS) (r=+0.60 and p=<0.001), quantitative myasthenia gravis score (QMGS) (r=+0.56 and p=0.01), and GBS disability scale (GDS) (r=+0.37 and p=0.04). Taken together, our findings suggest that complement activation mediated by MBL contributes to the pathogenesis and also severity of MS, MG, and GBS. However, because the lectin pathway can be involved in several phases of the immune response, further evidence will be required to elucidate the underlying mechanism.
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topic |
Autoimmunity Complement system proteins Guillain-Barre syndrome Mannose-binding lectin Multiple sclerosis Myasthenia gravis |
url |
https://ijaai.tums.ac.ir/index.php/ijaai/article/view/645 |
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