Myelin lipids in the development of the autoimmune response in multiple sclerosis

2014 ◽  
Vol 8 (4) ◽  
pp. 231-237
Author(s):  
M. V. Ivanova ◽  
A. I. Tukhvatulin ◽  
A. Sh. Dzharullaeva ◽  
D. Yu. Logunov ◽  
M. N. Zakharova
Keyword(s):  
Multiple Sclerosis ◽  
Autoimmune Response ◽  
Myelin Lipids

scholarly journals Degenerate TCR recognition and dual DR2 restriction of autoreactive T cells: Implications for the initiation of the autoimmune response in multiple sclerosis

2008 ◽  
Vol 38 (5) ◽  
pp. 1297-1309 ◽  
Author(s):  
Xin Zhang ◽  
Yunan Tang ◽  
Danuta Sujkowska ◽  
Jinzhao Wang ◽  
Vinod Ramgolam ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
T Cells ◽  
Autoimmune Response ◽  
Autoreactive T Cells

scholarly journals GDP-l-fucose synthase is a CD4+ T cell–specific autoantigen in DRB3*02:02 patients with multiple sclerosis

2018 ◽  
Vol 10 (462) ◽  
pp. eaat4301 ◽  
Author(s):  
Raquel Planas ◽  
Radleigh Santos ◽  
Paula Tomas-Ojer ◽  
Carolina Cruciani ◽  
Andreas Lutterotti ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
T Cell ◽  
Cell Clone ◽  
Autoimmune Response ◽  
Guanosine Diphosphate ◽  
Immune Mediated ◽  
T Cell Clone ◽  
Positional Scanning ◽  
The Central Nervous System

Multiple sclerosis is an immune-mediated autoimmune disease of the central nervous system that develops in genetically susceptible individuals and likely requires environmental triggers. The autoantigens and molecular mimics triggering the autoimmune response in multiple sclerosis remain incompletely understood. By using a brain-infiltrating CD4+ T cell clone that is clonally expanded in multiple sclerosis brain lesions and a systematic approach for the identification of its target antigens, positional scanning peptide libraries in combination with biometrical analysis, we have identified guanosine diphosphate (GDP)–l-fucose synthase as an autoantigen that is recognized by cerebrospinal fluid–infiltrating CD4+ T cells from HLA-DRB3*–positive patients. Significant associations were found between reactivity to GDP-l-fucose synthase peptides and DRB3*02:02 expression, along with reactivity against an immunodominant myelin basic protein peptide. These results, coupled with the cross-recognition of homologous peptides from gut microbiota, suggest a possible role of this antigen as an inducer or driver of pathogenic autoimmune responses in multiple sclerosis.

scholarly journals Molecular Interventions towards Multiple Sclerosis Treatment

2020 ◽  
Vol 10 (5) ◽  
pp. 299
Author(s):  
Athanasios Metaxakis ◽  
Dionysia Petratou ◽  
Nektarios Tavernarakis
Keyword(s):  
Multiple Sclerosis ◽  
Autoimmune Response ◽  
Th2 Cells ◽  
Autoimmune Encephalomyelitis ◽  
T Helper 2 ◽  
Cellular Factors ◽  
Life Threatening ◽  
The Central Nervous System ◽  
Multiple Sclerosis Treatment ◽  
Molecular Interventions

Multiple sclerosis (MS) is an autoimmune life-threatening disease, afflicting millions of people worldwide. Although the disease is non-curable, considerable therapeutic advances have been achieved through molecular immunotherapeutic approaches, such as peptides vaccination, administration of monoclonal antibodies, and immunogenic copolymers. The main aims of these therapeutic strategies are to shift the MS-related autoimmune response towards a non-inflammatory T helper 2 (Th2) cells response, inactivate or ameliorate cytotoxic autoreactive T cells, induce secretion of anti-inflammatory cytokines, and inhibit recruitment of autoreactive lymphocytes to the central nervous system (CNS). These approaches can efficiently treat autoimmune encephalomyelitis (EAE), an essential system to study MS in animals, but they can only partially inhibit disease progress in humans. Nevertheless, modern immunotherapeutic techniques remain the most promising tools for the development of safe MS treatments, specifically targeting the cellular factors that trigger the initiation of the disease.

scholarly journals The Influence of Reactive Oxygen Species in the Immune System and Pathogenesis of Multiple Sclerosis

2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Mohammad javad Tavassolifar ◽  
Mohammad Vodjgani ◽  
Zahra Salehi ◽  
Maryam Izad
Keyword(s):  
Multiple Sclerosis ◽  
Reactive Oxygen Species ◽  
Immune System ◽  
T Cell ◽  
Reactive Oxygen ◽  
Autoimmune Response ◽  
Antioxidant Systems ◽  
Enzymatic Antioxidants ◽  
Oxygen Species ◽  
Nonenzymatic Antioxidants

Multiple roles have been indicated for reactive oxygen species (ROS) in the immune system in recent years. ROS have been extensively studied due to their ability to damage DNA and other subcellular structures. Noticeably, they have been identified as a pivotal second messenger for T-cell receptor signaling and T-cell activation and participate in antigen cross-presentation and chemotaxis. As an agent with direct toxic effects on cells, ROS lead to the initiation of the autoimmune response. Moreover, ROS levels are regulated by antioxidant systems, which include enzymatic and nonenzymatic antioxidants. Enzymatic antioxidants include superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase. Nonenzymatic antioxidants contain vitamins C, A, and E, glutathione, and thioredoxin. Particularly, cellular antioxidant systems have important functions in maintaining the redox system homeostasis. This review will discuss the significant roles of ROS generation and antioxidant systems under normal conditions, in the immune system, and pathogenesis of multiple sclerosis.

Systemic upregulation of CD40 and CD40 ligand mRNA expression in multiple sclerosis

2000 ◽  
Vol 6 (2) ◽  
pp. 61-65 ◽  
Author(s):  
Wen-Xin Huang ◽  
Ping Huang ◽  
Jan Hillert
Keyword(s):  
Multiple Sclerosis ◽  
Mononuclear Cells ◽  
Cd40 Ligand ◽  
Autoimmune Response ◽  
Mrna Levels ◽  
Healthy Controls ◽  
Peripheral Blood Mononuclear ◽  
Humoral Immune ◽  
Humoral Immune Responses ◽  
Organ Specific

It is increasingly clear that the CD40 and CD40 ligand (CD40L) receptor-ligand pair mediates a crucial activation signal in both cell-mediated and humoral immune responses. Here, we detected mRNA levels of CD40 and CD40L in non-stimulated peripheral blood mononuclear cells in 46 patients with multiple sclerosis (MS) and 46 healthy controls by a competitive RT-PCR procedure allowing quantification without previous culture or antigenic stimulation. The levels of CD40 and CD40L mRNA were markedly increased in MS patients (P <0.0001) compared with healthy controls. There was no difference between clinical MS subgroups or stage of disease. Our findings indicate that, although MS is an organ specific disorder an increased signaling via the CD40 and CD40L pathway may be present at the systemic level. The nature of this upregulation, whether primary or secondary to the organ-specific autoimmune response, is yet to be determined. Since interference with CD40/CD40L is an effective way to interfere with autoimmune model diseases such as experimental autoimmune encephalomyelitis, it may be relevant to investigate further the role of these molecules in the pathogenesis of MS.

Is There a Case for a Virus Aetiology in Multiple Sclerosis?

1995 ◽  
Vol 40 (2) ◽  
pp. 55-62 ◽  
Author(s):  
Bernard E. Souberbielle ◽  
Paul W.S. Szawlowski ◽  
William C. Russell
Keyword(s):  
Multiple Sclerosis ◽  
Demyelinating Disease ◽  
Autoimmune Response ◽  
Aggressive Approach ◽  
Shetland Islands ◽  
North East ◽  
High Prevalence ◽  
Specific Virus ◽  
Very High

Multiple Sclerosis (MS) is a devastating demyelinating disease with a very high prevalence in North-East Scotland and in the Orkney and Shetland Islands. MS appears to be a multifactorial disorder with environmental and genetic elements and it has been proposed that these, in tandem, provoke an autoimmune response giving rise to the disease. Although there is no direct evidence of a specific virus being involved in MS, there are nevertheless grounds for suspecting a viral association. This review discusses these aspects of MS and suggests that a more aggressive approach to unravelling the role of viruses is needed.

scholarly journals Sperm-Associated Antigen 16 Is a Novel Target of the Humoral Autoimmune Response in Multiple Sclerosis

2014 ◽  
Vol 193 (5) ◽  
pp. 2147-2156 ◽  
Author(s):  
Laura de Bock ◽  
Klaartje Somers ◽  
Judith Fraussen ◽  
Jerome J.A. Hendriks ◽  
Jack van Horssen ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Autoimmune Response ◽  
Novel Target

IFN-β treatment modulates the CD28/CTLA-4-mediated pathway for IL-2 production in patients with relapsing -remitting multiple sclerosis

2004 ◽  
Vol 10 (6) ◽  
pp. 630-635 ◽  
Author(s):  
C Espejo ◽  
L Brieva ◽  
G Ruggiero ◽  
J Río ◽  
X Montalban ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Chronic Inflammatory Disease ◽  
Autoimmune Response ◽  
T Cell Proliferation ◽  
Immunomodulatory Effects ◽  
Cd25 Expression ◽  
Relapsing Remitting ◽  
The Central Nervous System ◽  
Relapsing Remitting Multiple Sclerosis

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system probably mediated by Th1 lymphocytes. IFN-b is an established therapy for relapsing MS patients, although the mechanisms underlying its efficacy are yet to be well characterized. We determined IL-2 production, CD25 expression and T-cell proliferation from relapsing -remitting MS patients before and three months after starting therapy. A decrease in the percentage of CD80-induced IL-2-producing cells was observed after in vivo IFN-b treatment. These data support that one of the immunomodulatory effects of IFN-b treatment in MS may be a limitation of the autoimmune response modifying the CD80:CD28/CTLA-4 pathway.

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