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Article ; Online: Reply to "Myelin Oligodendrocyte Glycoprotein Antibody-Positive Patients Meeting the 2017 McDonald Criteria for Multiple Sclerosis: Challenges in Diagnosis and Treatment Decisions".

Villacieros-Álvarez, Javier / Espejo, Carmen / Cobo-Calvo, Álvaro

2023 Volume 95, Issue 2, Page(s) 415–416

MeSH term(s)	Humans ; Multiple Sclerosis/diagnosis ; Multiple Sclerosis/therapy ; Myelin-Oligodendrocyte Glycoprotein ; Autoantibodies ; Brain
Chemical Substances	Myelin-Oligodendrocyte Glycoprotein ; Autoantibodies
Language	English
Publishing date	2023-12-23
Publishing country	United States
Document type	Letter
ZDB-ID	80362-5
ISSN	1531-8249 ; 0364-5134
ISSN (online)	1531-8249
ISSN	0364-5134
DOI	10.1002/ana.26856
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Zs.A 1370: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 478: Show issues

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Article ; Online: Correcting gut dysbiosis can ameliorate inflammation and promote remyelination in multiple sclerosis - Yes.

Calvo-Barreiro, Laura / Clerico, Marinella / Espejo, Carmen

Multiple sclerosis (Houndmills, Basingstoke, England)

2021 Volume 27, Issue 8, Page(s) 1161–1162

MeSH term(s)	Dysbiosis ; Gastrointestinal Microbiome ; Humans ; Inflammation ; Multiple Sclerosis/drug therapy ; Remyelination
Language	English
Publishing date	2021-05-28
Publishing country	England
Document type	Journal Article
ZDB-ID	1290669-4
ISSN	1477-0970 ; 1352-4585
ISSN (online)	1477-0970
ISSN	1352-4585
DOI	10.1177/13524585211016723
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Article ; Online: Therapeutic Effect of IL-21 Blockage by Gene Therapy in Experimental Autoimmune Encephalomyelitis.

Edo, Ángel / Calvo-Barreiro, Laura / Eixarch, Herena / Bosch, Assumpció / Chillón, Miguel / Espejo, Carmen

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

2022 Volume 19, Issue 5, Page(s) 1617–1633

Abstract: The pathogenic role of the interleukin 21 (IL-21) in different autoimmune diseases, such as multiple sclerosis (MS), has been extensively studied. However, its pleiotropic nature makes it a cytokine that may exhibit different activity depending on the ... ...

Abstract	The pathogenic role of the interleukin 21 (IL-21) in different autoimmune diseases, such as multiple sclerosis (MS), has been extensively studied. However, its pleiotropic nature makes it a cytokine that may exhibit different activity depending on the immunological stage of the disease. In this study, we developed a gene therapy strategy to block the interaction between IL-21 and its receptor (IL-21R) by using adeno-associated vectors (AAV) encoding a new soluble cytokine receptor (sIL21R) protein. We tested this strategy in a murine model of experimental autoimmune encephalomyelitis (EAE), obtaining different clinical effects depending on the time at which the treatment was applied. Although the administration of the treatment during the development of the immune response was counterproductive, the preventive administration of the therapeutic vectors showed a protective effect by reducing the number of animals that developed the disease, as well as an improvement at the histopathological level and a modification of the immunological profile of the animals treated with the AAV8.sIL21R. The beneficial effect of the treatment was also observed when inducing the expression of the therapeutic molecule once the first neurological signs were established in a therapeutic approach with a doxycyline (Dox)-inducible expression system. All these clinical results highlight the pleiotropicity of this cytokine in the different clinical stages and its key role in the EAE immunopathogenesis.
MeSH term(s)	Animals ; Mice ; Encephalomyelitis, Autoimmune, Experimental/genetics ; Encephalomyelitis, Autoimmune, Experimental/therapy ; Mice, Inbred C57BL ; Multiple Sclerosis/genetics ; Multiple Sclerosis/therapy ; Genetic Therapy/methods ; Cytokines/genetics ; Receptors, Cytokine/genetics ; Receptors, Cytokine/therapeutic use
Chemical Substances	interleukin-21 (MKM3CA6LT1) ; Cytokines ; Receptors, Cytokine
Language	English
Publishing date	2022-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2316693-9
ISSN	1878-7479 ; 1933-7213
ISSN (online)	1878-7479
ISSN	1933-7213
DOI	10.1007/s13311-022-01279-8
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Article ; Online: Immunosenescence in multiple sclerosis: the identification of new therapeutic targets.

Dema, María / Eixarch, Herena / Villar, Luisa M / Montalban, Xavier / Espejo, Carmen

Autoimmunity reviews

2021 Volume 20, Issue 9, Page(s) 102893

Abstract: The number of elderly multiple sclerosis (MS) patients is growing, mainly due to the increase in the life expectancy of the general population and the availability of effective disease-modifying treatments. However, current treatments reduce the ... ...

Abstract	The number of elderly multiple sclerosis (MS) patients is growing, mainly due to the increase in the life expectancy of the general population and the availability of effective disease-modifying treatments. However, current treatments reduce the frequency of relapses and slow the progression of the disease, but they cannot stop the disability accumulation associated with disease progression. One possible explanation is the impact of immunosenescence, which is associated with the accumulation of unusual immune cell subsets that are thought to have a role in the development of an early ageing process in autoimmunity. Here, we provide a recent overview of how senescence affects immune cell function and how it is involved in the pathogenesis of autoimmune diseases, particularly MS. Numerous studies have demonstrated age-related immune changes in experimental autoimmune encephalomyelitis models, and the premature onset of immunosenescence has been demonstrated in MS patients. Therefore, potential therapeutic strategies based on rejuvenating the immune system have been proposed. Senolytics and regenerative strategies using haematopoietic stem cells, therapies based on rejuvenating oligodendrocyte precursor cells, microglia and monocytes, thymus cells and senescent B and T cells are capable of reversing the process of immunosenescence and could have a beneficial impact on the progression of MS.
MeSH term(s)	Aged ; Animals ; Autoimmunity ; Encephalomyelitis, Autoimmune, Experimental/therapy ; Humans ; Immunosenescence ; Multiple Sclerosis/therapy ; T-Lymphocytes
Language	English
Publishing date	2021-07-05
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2144145-5
ISSN	1873-0183 ; 1568-9972
ISSN (online)	1873-0183
ISSN	1568-9972
DOI	10.1016/j.autrev.2021.102893
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Article ; Online: Molecular signature associated with cladribine treatment in patients with multiple sclerosis.

Fissolo, Nicolas / Calvo-Barreiro, Laura / Eixarch, Herena / Boschert, Ursula / Villar, Luisa M / Costa-Frossard, Lucienne / Ferrer, Mireia / Sanchez, Alex / Borràs, Eva / Sabidó, Eduard / Espejo, Carmen / Montalban, Xavier / Comabella, Manuel

Frontiers in immunology

2023 Volume 14, Page(s) 1233546

Abstract: Introduction: Little is known about the molecular profiling associated with the effect of cladribine in patients with multiple sclerosis (MS). Here, we aimed first to characterize the transcriptomic and proteomic profiles induced by cladribine in blood ... ...

Abstract	Introduction: Little is known about the molecular profiling associated with the effect of cladribine in patients with multiple sclerosis (MS). Here, we aimed first to characterize the transcriptomic and proteomic profiles induced by cladribine in blood cells, and second to identify potential treatment response biomarkers to cladribine in patients with MS. Methods: Gene, protein and microRNA (miRNA) expression profiles were determined by microarrays (genes, miRNAs) and mass spectrometry (proteins) in peripheral blood mononuclear cells (PBMCs) from MS patients after Results: PBMCs treated Discussion: By using a combination of omics data and bioinformatics approaches we were able to identify a multiomics molecular profile induced by cladribine
MeSH term(s)	Humans ; Cladribine/pharmacology ; Cladribine/therapeutic use ; Multiple Sclerosis/drug therapy ; Multiple Sclerosis/genetics ; Multiple Sclerosis/metabolism ; Leukocytes, Mononuclear/metabolism ; Proteomics ; MicroRNAs/metabolism ; Biomarkers
Chemical Substances	Cladribine (47M74X9YT5) ; MicroRNAs ; Biomarkers
Language	English
Publishing date	2023-07-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1233546
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Article ; Online: Non-ADEM encephalitis in patients with myelin oligodendrocyte glycoprotein antibodies: a systematic review.

Vega, Enrique / Arrambide, Georgina / Olivé, Gemma / Castillo, Mireia / Felipe-Rucián, Ana / Tintoré, Mar / Montalban, Xavier / Espejo, Carmen / Sepúlveda, María / Armangué, Thais / Cobo-Calvo, Alvaro

European journal of neurology

2023 Volume 30, Issue 5, Page(s) 1515–1527

Abstract: Background and purpose: Non-(acute disseminated encephalomyelitis) (non-ADEM) encephalitis and/or fluid attenuated inversion recovery hyperintense lesions in anti-myelin-oligodendrocyte-glycoprotein-associated encephalitis with seizures (FLAMES) are ... ...

Abstract	Background and purpose: Non-(acute disseminated encephalomyelitis) (non-ADEM) encephalitis and/or fluid attenuated inversion recovery hyperintense lesions in anti-myelin-oligodendrocyte-glycoprotein-associated encephalitis with seizures (FLAMES) are rarely described in patients with myelin oligodendrocyte glycoprotein (MOG) antibodies (Abs). The aim was (i) to describe the clinical features and disease course of children and adults with non-ADEM encephalitis and/or FLAMES associated with MOG Abs and (ii) to describe their association with other central nervous system autoantibodies. Methods: This was a systematic review following the PRISMA guidelines. Patients fulfilled criteria for non-ADEM encephalitis and/or FLAMES, and all were MOG Ab positive. Results: In total, 83 (79%) patients with non-ADEM encephalitis (48 also had FLAMES) and 22 (21%) with isolated FLAMES were included. At the first episode, children (n = 45) had more infections (11/45, 24.4%; p = 0.017) and more of the phenotype consisting of non-ADEM encephalitis (42/45, 93.3%; p = 0.014) than adults (n = 38). Children had more episodes consistent with working memory deficits (25/54, 46.3%; p = 0.014) but fewer psychiatric symptoms (16/54, 29.6%; p = 0.002). Twenty-eight (40.6%) of 69 patients had N-methyl-d-aspartate receptor (NMDAR) Abs in cerebrospinal fluid (CSF), being more frequent in adults (19/29, 65.5%; p < 0.001). Compared to negatives, positive CSF NMDAR Abs had more relapses (14/20, 70%; p = 0.050), required ventilatory support more frequently (8/34, 23.5%; p = 0.009) and had more psychiatric episodes (28/34, 82%; p < 0.001) or abnormal movements (14/34, 41.2%; p = 0.008). Apart from an older age in FLAMES, positive and negative CSF NMDAR Ab groups shared similar features. Conclusion: Non-ADEM encephalitis patients with MOG Abs show specific clinical and radiological features, depending on the age at first episode. The presence of MOG Abs in non-ADEM encephalitis patients should not rule out to test other autoantibodies, especially concomitant NMDAR Abs in patients with suggestive symptoms such as behavioural or movement alterations.
MeSH term(s)	Humans ; Myelin-Oligodendrocyte Glycoprotein ; Encephalitis ; Encephalomyelitis, Acute Disseminated ; Disease Progression ; Autoantibodies
Chemical Substances	Myelin-Oligodendrocyte Glycoprotein ; Autoantibodies
Language	English
Publishing date	2023-02-20
Publishing country	England
Document type	Systematic Review ; Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1280785-0
ISSN	1468-1331 ; 1351-5101 ; 1471-0552
ISSN (online)	1468-1331
ISSN	1351-5101 ; 1471-0552
DOI	10.1111/ene.15684
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Zs.A 4738: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Combined therapies to treat complex diseases: The role of the gut microbiota in multiple sclerosis.

Calvo-Barreiro, Laura / Eixarch, Herena / Montalban, Xavier / Espejo, Carmen

Autoimmunity reviews

2018 Volume 17, Issue 2, Page(s) 165–174

Abstract: The commensal microbiota has emerged as an environmental risk factor for multiple sclerosis (MS). Studies in experimental autoimmune encephalomyelitis (EAE) models have shown that the commensal microbiota is an essential player in triggering autoimmune ... ...

Abstract	The commensal microbiota has emerged as an environmental risk factor for multiple sclerosis (MS). Studies in experimental autoimmune encephalomyelitis (EAE) models have shown that the commensal microbiota is an essential player in triggering autoimmune demyelination. Likewise, the commensal microbiota modulates the host immune system, alters the integrity and function of biological barriers and has a direct effect on several types of central nervous system (CNS)-resident cells. Moreover, a characteristic gut dysbiosis has been recognized as a consistent feature during the clinical course of MS, and the MS-related microbiota is gradually being elucidated. This review highlights animal studies in which commensal microbiota modulation was tested in EAE, as well as the mechanisms of action and influence of the commensal microbiota not only in the local milieu but also in the innate and adaptive immune system and the CNS. Regarding human research, this review focuses on studies that show how the commensal microbiota might act as a pathogenic environmental risk factor by directing immune responses towards characteristic pathogenic profiles of MS. We speculate how specific microbiome signatures could be obtained and used as potential pathogenic events and biomarkers for the clinical course of MS. Finally, we review recently published and ongoing clinical trials in MS patients regarding the immunomodulatory properties exerted by some microorganisms. Because MS is a complex disease with a large variety of associated environmental risk factors, we suggest that current treatments combined with strategies that modulate the commensal microbiota would constitute a broader immunotherapeutic approach and improve the clinical outcome for MS patients.
MeSH term(s)	Animals ; Dysbiosis/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Gastrointestinal Microbiome/immunology ; Humans ; Mice ; Microbiota/immunology ; Multiple Sclerosis/immunology
Language	English
Publishing date	2018-02
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2144145-5
ISSN	1873-0183 ; 1568-9972
ISSN (online)	1873-0183
ISSN	1568-9972
DOI	10.1016/j.autrev.2017.11.019
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Article ; Online: Immunomodulatory Effects Associated with Cladribine Treatment.

Fissolo, Nicolás / Calvo-Barreiro, Laura / Eixarch, Herena / Boschert, Ursula / Espejo, Carmen / Montalban, Xavier / Comabella, Manuel

Cells

2021 Volume 10, Issue 12

Abstract: Cladribine is a synthetic deoxyadenosine analogue with demonstrated efficacy in patients with relapsing-remitting multiple sclerosis (MS). The main mechanism of action described for cladribine is the induction of a cytotoxic effect on lymphocytes, ... ...

Abstract	Cladribine is a synthetic deoxyadenosine analogue with demonstrated efficacy in patients with relapsing-remitting multiple sclerosis (MS). The main mechanism of action described for cladribine is the induction of a cytotoxic effect on lymphocytes, leading to a long-term depletion of peripheral T and B cells. Besides lymphocyte toxicity, the mode of action may include immunomodulatory mechanisms affecting other cells of the immune system. In order to induce its beneficial effects, cladribine is phosphorylated inside the cell by deoxycytidine kinase (DCK) to its active form. However, the mechanism of action of cladribine may also include immunomodulatory pathways independent of DCK activation. This in vitro study was designed to explore the impact of cladribine on peripheral blood mononuclear cells (PBMC) subsets, and to assess whether the immunomodulatory mechanisms induced by cladribine depend on the activation of the molecule. To this end, we obtained PBMCs from healthy donors and MS patients and performed proliferation, apoptosis and activation assays with clinically relevant concentrations of cladribine in DCK-dependent and -independent conditions. We also evaluated the effect of cladribine on myeloid lineage-derived cells, monocytes and dendritic cells (DCs). Cladribine decreased proliferation and increased apoptosis of lymphocyte subsets after prodrug activation via DCK. In contrast, cladribine induced a decrease in immune cell activation through both DCK-dependent and -independent pathways (not requiring prodrug activation). Regarding monocytes and DCs, cladribine induced cytotoxicity and impaired the activation of classical monocytes, but had no effect on DC maturation. Taken together, these data indicate that cladribine, in addition to its cytotoxic function, can mediate immunomodulation in different immune cell populations, by regulating their proliferation, maturation and activation.
MeSH term(s)	Apoptosis/drug effects ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Cladribine/pharmacology ; Deoxycytidine Kinase/metabolism ; Humans ; Immunomodulation/drug effects ; Leukocytes, Mononuclear/drug effects ; Leukocytes, Mononuclear/metabolism ; Lipopolysaccharides/pharmacology ; Monocytes/drug effects ; Monocytes/metabolism ; Prodrugs/pharmacology
Chemical Substances	Lipopolysaccharides ; Prodrugs ; Cladribine (47M74X9YT5) ; Deoxycytidine Kinase (EC 2.7.1.74)
Language	English
Publishing date	2021-12-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10123488
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Article ; Online: Dalfampridine in multiple sclerosis: from symptomatic treatment to immunomodulation.

Espejo, Carmen / Montalban, Xavier

Clinical immunology (Orlando, Fla.)

2012 Volume 142, Issue 1, Page(s) 84–92

Abstract: Multiple sclerosis (MS) is a neurodegenerative disease that is deemed to affect more than 2.1 million people worldwide, and for which there is no cure. Early symptoms of MS are believed to result from axonal demyelination leading to slowing or blockade ... ...

Abstract	Multiple sclerosis (MS) is a neurodegenerative disease that is deemed to affect more than 2.1 million people worldwide, and for which there is no cure. Early symptoms of MS are believed to result from axonal demyelination leading to slowing or blockade of impulse conduction. The blockade of K+ channels has been proven to improve conduction deficiencies secondary to demyelination in patients with MS. Dalfampridine is a K+ channel blocker that was recently approved by FDA for the symptomatic treatment of ambulation hardship in MS. Understanding the mechanisms by which Dalfampridine exerts its therapeutic effects is a complex issue as it blocks a wide variety of K+ channels that are distributed across multiple cell types in the nervous system but also in the immune system, and because of their molecular identities remaining unknown. This review describes Dalfampridine potential roles at the cellular and molecular levels in MS pathogenesis.
MeSH term(s)	4-Aminopyridine/pharmacology ; Clinical Trials as Topic ; Humans ; Immunologic Factors/pharmacology ; Immunomodulation/immunology ; Multiple Sclerosis/drug therapy ; Potassium Channel Blockers/pharmacology
Chemical Substances	Immunologic Factors ; Potassium Channel Blockers ; 4-Aminopyridine (BH3B64OKL9)
Language	English
Publishing date	2012-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2011.06.004
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Zs.A 880: Show issues

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Article ; Online: Bone morphogenetic proteins in multiple sclerosis: Role in neuroinflammation.

Eixarch, Herena / Calvo-Barreiro, Laura / Montalban, Xavier / Espejo, Carmen

Brain, behavior, and immunity

2017 Volume 68, Page(s) 1–10

Abstract: Bone morphogenetic proteins (BMPs) are growth factors that represent the largest subgroup of signalling ligands of the transforming growth factor beta (TGF-β) superfamily. Their participation in the proliferation, survival and cell fate of several cell ... ...

Abstract	Bone morphogenetic proteins (BMPs) are growth factors that represent the largest subgroup of signalling ligands of the transforming growth factor beta (TGF-β) superfamily. Their participation in the proliferation, survival and cell fate of several cell types and their involvement in many pathological conditions are now well known. BMP expression is altered in multiple sclerosis (MS) patients, suggesting that BMPs have a role in the pathogenesis of this disease. MS is a demyelinating and neurodegenerative autoimmune disorder of the central nervous system (CNS). MS is a complex pathological condition in which genetic, epigenetic and environmental factors converge, although its aetiology remains elusive. Multifunctional molecules, such as BMPs, are extremely interesting in the field of MS because they are involved in the regulation of several adult tissues, including the CNS and the immune system. In this review, we discuss the extensive data available regarding the role of BMP signalling in neuronal progenitor/stem cell fate and focus on the participation and expression of BMPs in CNS demyelination. Additionally, we provide an overview of the involvement of BMPs as modulators of the immune system, as this subject has not been thoroughly explored even though it is of great interest in autoimmune disorders. Moreover, we describe the data on BMP signalling in autoimmunity and inflammatory diseases, including MS and its experimental models. Thus, we aim to provide an integrated view of the putative role of BMPs in MS pathogenesis and to open the field for the further development of alternative therapeutic strategies for MS patients.
MeSH term(s)	Autoimmunity/physiology ; Bone Morphogenetic Proteins/genetics ; Bone Morphogenetic Proteins/metabolism ; Bone Morphogenetic Proteins/physiology ; Cell Differentiation ; Cell Lineage ; Central Nervous System/metabolism ; Demyelinating Diseases ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Humans ; Multiple Sclerosis/pathology ; Neuroglia ; Neuroimmunomodulation/physiology ; Neurons ; Signal Transduction
Chemical Substances	Bone Morphogenetic Proteins
Language	English
Publishing date	2017-02-27
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2017.02.019
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