Treating multiple sclerosis with monoclonal antibodies: a 2013 update

Deiß, Annika; Brecht, Isabel; Haarmann, Axel; Buttmann, Mathias

doi:10.1586/ern.13.17

Cited by 47 publications

(27 citation statements)

References 109 publications

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“…MS4A1 was found to interact with activated B cell antigen receptor complex (BCR) [29] and then leaded to the differentiation and activation of B cells [33]. Anti-MS4A1 antibodies target B cells have been proved to be the effective therapy for B cell lymphomas and some autoimmune diseases, including multiple sclerosis (MS) [34][35][36]. MS4A2 also has been conducted in relation to the degranulation of mast cells and cytokine release [37] and therefore has an important role in hypersensitivity and allergic reactions [38].…”

Section: Biochemical Properties Of Ms4a Gene Clustermentioning

confidence: 99%

MS4A Cluster in Alzheimer’s Disease

Tan

2014

Mol Neurobiol

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Several variants within membrane-spanning 4-domains subfamily A (MS4A) gene cluster have recently been implicated the association of Alzheimer's disease (AD) by serial recent genome-wide association studies (GWAS). As cell membrane proteins, MS4A family members are found to participate in the regulation of calcium signaling which have been widely discussed in neurodegeneration and AD. Besides, although the MS4A family members are poorly characterized, an important role in immunity has already been identified for several members of this cluster (such as MS4A1, MS4A2, and MS4A4B), indicating the possible involvement of MS4A gene cluster in AD pathogenesis. In this article, we briefly summarize the structure, localization, and function of MS4A gene cluster, review recent genetic and expression findings concerning the association of MS4A gene cluster with AD pathogenesis, and also speculate the possible roles of MS4A gene cluster in this disease. Based on the contributing effects of MS4A gene cluster in AD pathogenesis, targeting MS4A gene cluster might provide new opportunities for AD treatment.

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Section: Biochemical Properties Of Ms4a Gene Clustermentioning

confidence: 99%

MS4A Cluster in Alzheimer’s Disease

Tan

2014

Mol Neurobiol

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“…By inducing macrophages into a pro-inflammatory phenotype, CSF2 may contribute to inflammation. The expression of CSF2 is regulated by TNF and MIP-1A [15]. Exogenous CSF2 was reported to exacerbate collagen-induced arthritis and deficiency of CSF2 decreased the level of arthritis disease.…”

Section: Discussionmentioning

confidence: 99%

Insight into the Mechanism of SDS Irritation on Human Skin Keratinocytes by Examination of Changes in Gene Expression

Wang¹,

An²,

Zhao³

et al. 2016

Am. J. Biomed. Sci.

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Sodium dodecyl sulfate (SDS) is widely used as an irritant. Inflammatory and immune related cytokines/ chemokines are released by keratinocytes following SDS irritation. However, a specific effect of SDS on keratinocytes and the mechanism of skin irritation caused by SDS have not been investigated. To explore the irritant mechanism of SDS on keratinocytes, a gene microarray was used to detect the changes in gene expression after treating keratinocytes with SDS for different amounts of time. After 0.5 h and 1 h SDS exposure, there were changes mainly in genes in the rheumatoid arthritis pathway (CCL5, IL-6, FOS, CSF1, and HLA-DPB1) and TNF signaling pathway (TNF, CSF2, CXCL3, TNFAIP3, PTGS2, CXCL8, CCL20, and PIK3CA) to cause a pro-inflammatory reaction as well as autoimmune activation. After treating with SDS for 2 h and 4 h, there were changes in the expression of genes (LIF, PIM1, MAP3K8, CCNA1, RUNX1, and CYP1) that are related to cell apoptosis and cancerization. This was related to changes in transcriptional activity in the cancer and tryptophan metabolism pathway. Overall, SDS irritation caused different changes in gene expression over time, which altered the state of keratinocytes affecting processes of inflammation, autoimmune response, cell apoptosis, and cancerization. These results provide insight into the irritation process of SDS and provide reference for the future evaluation of skin irritation.

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“…24,25 Por otra parte, la administración de secukinumab (en fase IIa, un anticuerpo que neutraliza a IL17) reduce significativamente el nú-mero de lesiones en el SNC y muestra una tendencia a disminuir el número de brotes durante 6 meses. 26,27 Cabe destacar que las células Th1 y Th17 también promueven la activación de microglías, macrófagos, astrocitos y linfocitos B mediante la producción de citocinas y factores de crecimiento, activando mecanismos adicionales neurodegenerativos. Por ejemplo, las células Th1 y Th17 producen GM-CSF, el cual activa funciones neurodegenerativas de las microglías.…”

Section: Repuesta Inmunológica Localunclassified

Esclerosis múltiple: aspectos inmunológicos actuales

Cuevas-García¹

2017

RAM

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Multiple sclerosis is the most common inflammatory, chronic and degenerative condition of the central nervous system, and represents the first cause of disability in young adults. In Mexico, 11 to 20 out of every 100 000 people suffer from this disease. The causes of multiple sclerosis remain unknown, but several theories have been proposed: the interaction of environmental factors, viral infectious factors and genetic and immune susceptibility of each individual patient, which induce an autoimmune response and promote neuronal/axonal degeneration. In this review, the immune reaction main components and neurodegeneration present in multiple sclerosis are analyzed, as well as the inflammatory cascade associated with demyelination. Available treatments' main purpose is to modulate aspects related to the adaptive immune response (B and T cells). The therapeutic challenge will be antigen-specific immune-tolerance induction, for example, with the use of tolerance protocols with peptides or DNA or nanoparticles vaccines. Future therapies should aim to control innate components (microglia, macrophages, astrocytes) and to promote remyelination. To optimize the treatment, a combined therapeutic approach targeting the control of inflammatory and neurodegenerative components of the disease and monitoring of biomarkers will be necessary.

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Treating multiple sclerosis with monoclonal antibodies: a 2013 update

Cited by 47 publications

References 109 publications

MS4A Cluster in Alzheimer’s Disease

MS4A Cluster in Alzheimer’s Disease

Insight into the Mechanism of SDS Irritation on Human Skin Keratinocytes by Examination of Changes in Gene Expression

Esclerosis múltiple: aspectos inmunológicos actuales

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