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Multiple sclerosis immunology

Hans Lassmann, Monika Bradl
One of the most frequent statements, provided in different variations in the introduction of experimental studies on multiple sclerosis (MS), is that "Multiple sclerosis is a demyelinating autoimmune disease and experimental autoimmune encephalomyelitis (EAE) is a suitable model to study its pathogenesis". However, so far, no single experimental model covers the entire spectrum of the clinical, pathological, or immunological features of the disease. Many different models are available, which proved to be highly useful for studying different aspects of inflammation, demyelination, remyelination, and neurodegeneration in the central nervous system...
October 20, 2016: Acta Neuropathologica
Verónica Murta, Carina Ferrari
In recent decades, several neurodegenerative diseases have been shown to be exacerbated by systemic inflammatory processes. There is a wide range of literature that demonstrates a clear but complex relationship between the central nervous system (CNS) and the immunological system, both under naïve or pathological conditions. In diseased brains, peripheral inflammation can transform "primed" microglia into an "active" state, which can trigger stronger pathological responses. Demyelinating diseases are a group of neurodegenerative diseases characterized by inflammatory lesions associated with demyelination, which in turn induces axonal damage, neurodegeneration, and progressive loss of function...
2016: Advances in Experimental Medicine and Biology
Wai-Ping Lee, Barbara Willekens, Patrick Cras, Herman Goossens, Eva Martínez-Cáceres, Zwi N Berneman, Nathalie Cools
While emerging evidence indicates that dendritic cells (DC) play a central role in the pathogenesis of multiple sclerosis (MS), their modulation with immunoregulatory agents provides prospect as disease-modifying therapy. Our observations reveal that 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) treatment of monocyte-derived DC results in a semimature phenotype and anti-inflammatory cytokine profile as compared to conventional DC, in both healthy controls and MS patients. Importantly, 1,25(OH)2D3-treated DC induce T cell hyporesponsiveness, as demonstrated in an allogeneic mixed leukocyte reaction...
2016: Journal of Immunology Research
Delgertsetseg Chuluundorj, Scott A Harding, David Abernethy, Anne Camille La Flamme
Multiple sclerosis (MS) is an immune-mediated disease of the CNS, and monocytes contribute to MS-associated neuroinflammation. While classically-activated monocytes promote inflammation, type II-activated monocytes improve the course of MS. This study investigated type II activation of monocytes and their two main subsets, namely CD14(+) (CD14(++)CD16(-)subset) and CD16(+) monocytes (CD14(+)CD16(+)subset), by glatiramer acetate (GA) or intravenous immunoglobulin (IVIG)-associated immune complexes (IC), both of which are known MS treatments...
October 3, 2016: Immunology and Cell Biology
Sherry Freiesleben, Michael Hecker, Uwe Klaus Zettl, Georg Fuellen, Leila Taher
MicroRNAs (miRNAs) have been reported to contribute to the pathophysiology of multiple sclerosis (MS), an inflammatory disorder of the central nervous system. Here, we propose a new consensus-based strategy to analyse and integrate miRNA and gene expression data in MS as well as other publically available data to gain a deeper understanding of the role of miRNAs in MS and to overcome the challenges posed by studies with limited patient sample sizes. We processed and analysed microarray datasets, and compared the expression of genes and miRNAs in the blood of MS patients and controls...
October 3, 2016: Scientific Reports
Anderson P Jones, Allan G Kermode, Robyn M Lucas, William M Carroll, David Nolan, Prue H Hart
Circulating T and B lymphocytes contribute to the pathogenesis of the neuroinflammatory autoimmune disease, multiple sclerosis (MS). Further progress in the development of MS treatments is dependent upon a greater understanding of the immunological disturbances that underlie the disease. Analyses of circulating immune cells by flow cytometry have revealed MS-associated alterations in the composition and function of T and B cell subsets, including temporal changes associated with disease activity. Disturbances in circulating immune populations reflect those observed in the central nervous system and include skewing towards proinflammatory CD4+ and CD8+ T cells and B cells, greater proportions of follicular T helper cells, and functional defects in the corresponding T and B regulatory subsets...
September 30, 2016: Clinical and Experimental Immunology
Xiao Liu, Haihong Qin, Jinhua Xu
Autophagy is a highly conserved catabolic process, whereby unwanted cytoplasmic contents are enclosed by the double-membrane autophagosomes and delivered to the lysosomes for degradation. It is responsible for the recycling of nutrients and cellular components, thus playing a pivotal role in maintaining cellular homeostasis as well as cell survival during stress conditions. Perturbations in autophagy are implicated in multiple diseases, such as cancers and neuro-degeneration diseases. Recent studies demonstrate that autophagy may participate in almost every step of immune responses, including pathogen recognition, antigen processing and presentation, immune cell development and function, and immunoregulation...
September 24, 2016: International Immunopharmacology
Daniel Kantor, Elias S Sotirchos, Peter A Calabresi
No abstract text is available yet for this article.
September 27, 2016: Neurology
Izumi Kawachi, Hans Lassmann
Multiple sclerosis (MS) and neuromyelitis optica (NMO) are autoimmune demyelinating diseases of the central nervous system (CNS), having distinct immunological and pathological features. They have two pathogenic components, 'inflammation' and 'neurodegeneration', with different degrees of severity and pathogenetic mechanisms. The target antigen of autoimmunity in NMO is the water channel aquaporin-4 (AQP4), and antibodies directed against this antigen result in astrocyte damage. MS is a disease primarily affecting myelin and oligodendrocytes, but thus far, no MS-specific autoantigen has been identified...
September 26, 2016: Journal of Neurology, Neurosurgery, and Psychiatry
Mohammad Reza Shiri-Shahsavar, Abbas Mirshafiee, Karim Parastouei, Abbas Ebrahimi-Kalan, Saeed Yekaninejad, Farid Soleymani, Reza Chahardoli, Ramin Mazaheri Nezhad Fard, Ali Akbar Saboor-Yaraghi
Vitamins are immunologically interesting due to their significant immunomodulatory activities. Experimental autoimmune encephalomyelitis (EAE) is one of the most commonly used experimental models for studying autoimmune disorder in multiple sclerosis (MS). The aim of this study was to evaluate the protective and ameliorative effects of novel combination of all-trans retinoic acid (ATRA), 1,25-dihydroxyvitamin D3 (D3), and docosahexaenoic acid (DHA) on EAE-specific determinants and target gene expressions. Mice were randomly categorized into three groups before EAE induction [non-treated EAE (Group E), treated EAE (Group T), and healthy mice (Group H)]...
September 19, 2016: Journal of Molecular Neuroscience: MN
Elena Grebenciucova, Anthony T Reder, Jacqueline T Bernard
BACKGROUND: Fingolimod is a disease-modifying agent used in the treatment of relapsing/remitting multiple sclerosis. In MS clinical studies, the overall rate of infections in fingolimod group was overall similar to placebo, except for slightly more common lower respiratory tract infections and to a lesser extent HSV. Recently, an increasing number of cryptococcal infections associated with a long-term use of this medication have been reported. METHODS: We reviewed literature for cases of cryptococcal infection associated with the use of fingolimod and reported a case at our institution, as well as carefully evaluated the established immune mechanisms of the medication and discussed new insights into its short-term and long-term immunologic effects that may become important in the context of risk of infection...
September 2016: Multiple Sclerosis and related Disorders
Louisane Desbiens, Catherine Lapointe, Marjan Gharagozloo, Shaimaa Mahmoud, Gunnar Pejler, Denis Gris, Pedro D'Orléans-Juste
Experimental autoimmune encephalomyelitis (EAE) is a mouse model that reproduces cardinal signs of clinical, histopathological, and immunological features found in Multiple Sclerosis (MS). Mast cells are suggested to be involved in the main inflammatory phases occurring during EAE development, possibly by secreting several autacoids and proteases. Among the latter, the chymase mouse mast cell protease 4 (mMCP-4) can contribute to the inflammatory response by producing endothelin-1 (ET-1). The aim of this study was to determine the impact of mMCP-4 on acute inflammatory stages in EAE...
2016: Mediators of Inflammation
Juliane Wolter, Lorenz Schild, Fabian Bock, Andrea Hellwig, Ihsan Gadi, Moh D Mohanad Al-Dabet, Satish Ranjan, Raik Rönicke, Peter P Nawroth, Karl-Uwe Petersen, Christian Mawrin, Khurrum Shahzad, Berend Isermann
BACKGROUND: Studies with human samples and in rodents established a function of coagulation proteases in neuro-inflammatory demyelinating diseases, e.g. in multiple sclerosis (MS) and experimental autoimmune encephalitis (EAE). Surprisingly, approaches to increase aPC plasma levels as well as antibody mediated inhibition of PC/aPC ameliorated EAE in mice. Hence, the role of aPC generation in demyelinating diseases and potential mechanisms involved remain controversial. Furthermore, it is not known whether loss of aPC has pathological consequences at baseline, e...
September 3, 2016: Journal of Thrombosis and Haemostasis: JTH
T Berger
In this review, the immune-to-brain communication pathways are briefly summarized, with emphasis on the impact of immune cells and their mediators on learning, memory and other cognitive domains. Further, the acute response of the central nervous system to peripherally generated inflammatory stimuli - termed as sickness behaviour - is described, and the central role of microglia in this immune-to-brain crosstalk in physiological and pathological conditions is highlighted. Finally, the role and consequences of immunological processes related to cognitive impairment in multiple sclerosis are discussed...
September 2016: Acta Neurologica Scandinavica
Lisa H Tostanoski, Yu-Chieh Chiu, James I Andorko, Ming Guo, Xiangbin Zeng, Peipei Zhang, Walter Royal Iii, Christopher M Jewell
Recent studies demonstrate that excess signaling through inflammatory pathways (e.g., toll-like receptors, TLRs) contributes to the pathogenesis of human autoimmune diseases, including lupus, diabetes, and multiple sclerosis (MS). We hypothesized that co-delivery of a regulatory ligand of TLR9, GpG oligonucleotide, along with myelin - the "self" molecule attacked in MS - might restrain the pro-inflammatory signaling typically present during myelin presentation, redirecting T cell differentiation away from inflammatory populations and towards tolerogenic phenotypes such as regulatory T cells...
August 31, 2016: ACS Nano
Maria Rodi, Nikolaos Dimisianos, Anne-Lise de Lastic, Panagiota Sakellaraki, George Deraos, John Matsoukas, Panagiotis Papathanasopoulos, Athanasia Mouzaki
Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) of autoimmune etiology that results from an imbalance between CNS-specific T effector cells and peripheral suppressive mechanisms mediated by regulatory cells (RC). In this research, we collected blood samples from 83 relapsing remitting MS (RRMS) patients and 45 healthy persons (HC), to assess the sizes of their RC populations, including CD4⁺CD25(high)Foxp3⁺ (nTregs), CD3⁺CD4⁺HLA(-)G⁺, CD3⁺CD8⁺CD28(-), CD3⁺CD56⁺, and CD56(bright) cells, and how RC are affected by disease activity (acute phase or remission) and types of treatment (methylprednisolone, interferon, or natalizumab)...
2016: International Journal of Molecular Sciences
Benjamin Ettle, Kristina Kuhbandner, Stefanie Jörg, Alana Hoffmann, Jürgen Winkler, Ralf A Linker
BACKGROUND: Increased α-synuclein immunoreactivity has been associated with inflammatory activity in multiple sclerosis (MS) lesions, but the function of α-synuclein in neuroinflammation remains unknown. The aim of this study was to examine the role of α-synuclein in immunological processes in murine experimental autoimmune encephalomyelitis (EAE) as a model of MS. FINDINGS: We studied EAE in wildtype (aSyn(+/+)) and α-synuclein knockout (aSyn(-/-)) mice on a C57BL/6N background...
2016: Journal of Neuroinflammation
Jenny Freitag, Luciana Berod, Thomas Kamradt, Tim Sparwasser
A continuous increase in the prevalence of autoimmune diseases is to be expected in the aging societies worldwide. Autoimmune disorders not only cause severe disability and chronic pain, but also lead to considerable socio-economic costs. Given that the current treatment options are not curative, have substantial side effects and a high percentage of non-responders, innovative options to the existing therapeutic armament against autoimmune diseases are urgently required. Accumulating evidence suggests that changes in the metabolism of immune cells are associated with, and contribute to the pathogenesis of autoimmunity...
October 11, 2016: Immunology and Cell Biology
Maria Di Bari, Giovanni Di Pinto, Marcella Reale, Guadalupe Mengod, Ada Maria Tata
Multiple sclerosis (MS) is an inflammatory and neurodegenerative disease of the central nervous system (CNS) characterized by leucocytes infiltration, demyelination, axonal degeneration and neuronal death. Although the etiology of MS is still unknown, inflammation and autoimmunity are considered to be key players of the disease. The severe alterations affecting the nervous system contribute to the motor and cognitive disabilities and are in large part dependent on severe inflammatory processes active in both central nervous system and immune system...
August 22, 2016: Central Nervous System Agents in Medicinal Chemistry
Dean M Wingerchuk, Brian G Weinshenker
Multiple sclerosis (MS) is a common, disabling, putatively autoimmune neurological disease with worldwide distribution. It typically begins as a relapsing disorder that later evolves to a secondary progressive phase. Inflammatory and neurodegenerative mechanisms seem to operate in both phases, but their relative contributions and interactions are incompletely understood. Disease modifying therapies (DMTs) approved for relapsing multiple sclerosis interfere with a variety of immunological mechanisms to reduce rates of relapse, accumulation of disease burden measured by magnetic resonance imaging (MRI), and decline in neurological function over the two to three year duration of typical randomized controlled trials...
August 22, 2016: BMJ: British Medical Journal
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