scholarly journals Antibody-Proteases in the Pathogenesis of Autoimmune Demyelination and Monitoring Patients with Multiple Sclerosis

10.5772/22779 ◽  
2011 ◽  
Author(s):  
Dmitry Kostyushev ◽  
Dmitry Gnatenko ◽  
Mikhail Paltsev ◽  
Aleksandr Gabibov ◽  
Sergey Suchkov
Keyword(s):  
Multiple Sclerosis ◽  
Autoimmune Demyelination

The innate immune adaptor MyD88 is dispensable for spontaneous autoimmune demyelination in a mouse model of multiple sclerosis

2013 ◽  
Vol 255 (1-2) ◽  
pp. 60-69 ◽  
Author(s):  
Aaron G. Wexler ◽  
Christine Frielle ◽  
Gregory Berry ◽  
Lynn R. Budgeon ◽  
Jennifer Baccon ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Mouse Model ◽  
Innate Immune ◽  
Autoimmune Demyelination

scholarly journals Serum Glutamate Is a Predictor for the Diagnosis of Multiple Sclerosis

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Gheyath Al Gawwam ◽  
Inas K. Sharquie
Keyword(s):  
Multiple Sclerosis ◽  
Area Under The Curve ◽  
The Body ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Operating Characteristics ◽  
Serum Samples ◽  
Elisa Technique ◽  
Autoimmune Demyelination ◽  
Serum Glutamate

One neurotransmitter, glutamate, has been implicated in the autoimmune demyelination seen in multiple sclerosis (MS). Glutamate is present in many tissues in the body, so consideration should be given to whether the serum level of glutamate is likely well correlated with the activity of the disease. This research aimed to compare the serum glutamate levels from patients diagnosed with MS with those from an age-matched control population. A review of this data could shed light upon whether the serum testing of glutamate using Enzyme-Linked Immunosorbent Assay (ELISA) is a reliable indicator of MS activity. Serum samples were obtained from 55 patients with different patterns of MS and from 25 healthy adults as a control group. The ELISA technique was used to determine the glutamate levels in the serum samples. The mean serum glutamate level for patients with MS was1.318±0.543 nmol/ml and that of the controls was0.873±0.341 nmol/ml. The serum glutamate levels showed an area under the curve via the receiver operating characteristics (ROC) of 0.738, which was significant (pvalue = 0.001). The present study is the first to establish a strong connection between the serum glutamate levels and MS patients, where there was statistically significant elevation of serum glutamate in MS patients; hence this elevation might be used as a monitor to help in the diagnosis of MS patients.

Insights into multiple sclerosis provided by non-coding RNAs: meeting summary from the symposium ‘Non-coding RNAs in autoimmune disorders of the central nervous system’ on 5 April 2013 in Warsaw, Poland

2014 ◽  
Vol 20 (11) ◽  
pp. 1439-1442 ◽  
Author(s):  
Marcin P Mycko ◽  
Howard L Weiner ◽  
Krzysztof W Selmaj
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Cell Biology ◽  
Potential Role ◽  
Mechanisms Of Action ◽  
Ribonucleic Acids ◽  
The Central Nervous System ◽  
Non Coding Rnas ◽  
Autoimmune Demyelination

More than 80% of the human genome is biochemically active, whereas less than 3% of the genome encodes proteins. The emerging field of non-coding ribonucleic acids (RNAs) that are products of the genome, but do not program proteins, has revolutionized our understanding of cell biology. This was followed by a growing interest in the role of non-coding RNAs in the pathogenesis of human diseases, including multiple sclerosis (MS). In April 2013, a symposium in Warsaw, Poland, was the first meeting entirely dedicated to advances in the understanding of the roles of various subclasses of non-coding RNAs and showcased their involvement in autoimmune demyelination and MS. New mechanisms of action of small non-coding RNAs, as well as the advent of long non-coding RNAs were discussed, including the potential role of non-coding RNAs as MS biomarkers and their use for therapeutic intervention in MS.

Gender differences in autoimmune demyelination in the mouse: Implications for multiple sclerosis

1996 ◽  
Vol 39 (6) ◽  
pp. 724-733 ◽  
Author(s):  
Rhonda R. Voskuhl ◽  
Hilda Pitchekian-Halabi ◽  
Allan Mackenzie-Graham ◽  
Henry F. McFarland ◽  
Cedric S. Raine
Keyword(s):  
Multiple Sclerosis ◽  
Gender Differences ◽  
Autoimmune Demyelination

scholarly journals A Clonal NG2-Glia Cell Response in a Mouse Model of Multiple Sclerosis

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1279 ◽  
Author(s):  
Sonsoles Barriola ◽  
Fernando Pérez-Cerdá ◽  
Carlos Matute ◽  
Ana Bribián ◽  
Laura López-Mascaraque
Keyword(s):  
Multiple Sclerosis ◽  
Brain Damage ◽  
Tissue Repair ◽  
Phenotypic Diversity ◽  
Demyelinating Diseases ◽  
Autoimmune Encephalomyelitis ◽  
Oligodendrocyte Precursor ◽  
Autoimmune Demyelination ◽  
The Brain ◽  
Experimental Autoimmune

NG2-glia, also known as oligodendrocyte precursor cells (OPCs), have the potential to generate new mature oligodendrocytes and thus, to contribute to tissue repair in demyelinating diseases like multiple sclerosis (MS). Once activated in response to brain damage, NG2-glial cells proliferate, and they acquire a reactive phenotype and a heterogeneous appearance. Here, we set out to investigate the distribution and phenotypic diversity of NG2-glia relative to their ontogenic origin, and whether there is a clonal NG2-glial response to lesion in an experimental autoimmune encephalomyelitis (EAE) murine model of MS. As such, we performed in utero electroporation of the genomic lineage tracer, StarTrack, to follow the fate of NG2-glia derived from single progenitors and to evaluate their response to brain damage after EAE induction. We then analyzed the dispersion of the NG2-glia derived clonally from single pallial progenitors in the brain of EAE mice. In addition, we examined several morphological parameters to assess the degree of NG2-glia reactivity in clonally-related cells. Our results reveal the heterogeneity of these progenitors and their cell progeny in a scenario of autoimmune demyelination, revealing the ontogenic phenomena at play in these processes.

scholarly journals Oligodendroglial connexin 47 regulates neuroinflammation upon autoimmune demyelination in a novel mouse model of multiple sclerosis

2020 ◽  
Vol 117 (4) ◽  
pp. 2160-2169 ◽  
Author(s):  
Yinan Zhao ◽  
Ryo Yamasaki ◽  
Hiroo Yamaguchi ◽  
Satoshi Nagata ◽  
Hayato Une ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Mhc Class Ii ◽  
Critical Role ◽  
Conditional Knockout ◽  
Gene Expressions ◽  
Autoimmune Encephalomyelitis ◽  
Th 17 ◽  
Chronic Relapsing Eae ◽  
Autoimmune Demyelination

In multiple sclerosis plaques, oligodendroglial connexin (Cx) 47 constituting main gap junction channels with astroglial Cx43 is persistently lost. As mice with Cx47 single knockout exhibit no demyelination, the roles of Cx47 remain undefined. We aimed to clarify the effects of oligodendroglia-specific Cx47 inducible conditional knockout (icKO) on experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein peptide (MOG35-55) in PLP/CreERT;Cx47fl/fl mice at 14 d after tamoxifen injection. Cx47 icKO mice demonstrated exacerbation of acute and chronic relapsing EAE with more pronounced demyelination than Cx47 flox (fl)/fl littermates. CD3+ T cells more abundantly infiltrated the spinal cord in Cx47 icKO than in Cx47 fl/fl mice throughout the acute to chronic phases. CXCR3-CCR6+CD4+ and IL17+IFNγ-CD4+ helper T (Th) 17 cells isolated from spinal cord and brain tissues were significantly increased in Cx47 icKO mice compared with Cx47 fl/fl mice, while MOG35-55-specific proliferation and proinflammatory cytokine production of splenocytes were unaltered. Microarray analysis of isolated microglia revealed stronger microglial activation toward proinflammatory and injury-response phenotypes with increased expressions of chemokines that can attract Th17 cells, including Ccl2, Ccl3, Ccl4, Ccl7, and Ccl8, in Cx47 icKO mice compared with Cx47 fl/fl mice. In Cx47 icKO mice, NOS2+ and MHC class II+ microglia were more enriched immunohistochemically, and A1-specific astroglial gene expressions and astroglia immunostained for C3, a representative A1 astrocyte marker, were significantly increased at the acute phase, compared with Cx47 fl/fl mice. These findings suggest that oligodendroglia-specific Cx47 ablation induces severe inflammation upon autoimmune demyelination, underscoring a critical role for Cx47 in regulating neuroinflammation.

scholarly journals microRNA and exosome profiling in multiple sclerosis

2020 ◽  
Vol 26 (5) ◽  
pp. 599-604
Author(s):  
Marcin P Mycko ◽  
Sergio E Baranzini
Keyword(s):  
Multiple Sclerosis ◽  
Cell Types ◽  
Experimental Models ◽  
Pharmacological Intervention ◽  
Disease Biomarkers ◽  
Cellular Processes ◽  
Sequencing Technologies ◽  
Non Coding Rna ◽  
Major Player ◽  
Autoimmune Demyelination

New DNA sequencing technologies have uncovered non-coding RNA (ncRNA) as a major player in regulating cellular processes and can no longer be dismissed as “junk” or “dark” RNA. Among the ncRNA, microRNA (miRNA) is arguably the most extensively characterized category and a number of studies have implicated them in regulating critical functions that can influence autoimmune demyelination. Of specific interest to multiple sclerosis (MS), miRNA have been implicated in both regulating immune responses and myelination, thus making them an attractive candidate for both pharmacological intervention and as disease biomarkers. In addition, exosomes, small vesicles secreted by most cell types and present in all body fluids, have been also shown to play roles in immune signaling, inflammation and angiogenesis. Therefore, exosomes are also being explored as tools for therapeutic delivery and as biomarkers. This article reviews the recent advances in miRNA and exosome profiling in MS and experimental models.

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