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Homo sapiens

ABSTRACT: Next Generation Sequencing of Pattern II Demyelinating Brain Lesions from a Multiple Sclerosis Patient

PROVIDER: PRJNA259873 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1561742.fastq.gz	Fastqsanger.gz
	SRR1561743.fastq.gz	Fastqsanger.gz
	SRR1561744.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing of Pattern II Demyelinating Brain Lesions from a Multiple Sclerosis Patient

Project description:Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system with marked heterogeneity in several aspects including pathological processes. Four histopathological patterns of MS have been described. Pattern II is characterized by infiltrating macrophages and T-cells and by antibody and complement deposition. Transcriptome analysis of three patern II demyelinating brain lesions from a multiple sclerosis patient using RNA sequencing demonstrated the presence of mRNA transcripts for genes specific of activated macrophages, T and B cells as well as genes coding for immunoglobulins, complement proteins and some pattern II associated proteins, providing additional evidence supporting pattern II demyelination. Examination of 3 different demyelinating lesions identified by Immunohistopathology.

2016-07-03 | E-GEOD-60942 | biostudies-arrayexpress

Multiple Sclerosis Pattern II Demyelinating Lesions

Project description:Multiple Sclerosis Pattern II Demyelinating Lesions

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Central Role of Th2 and Tc2 Lymphocytes in Multiple Sclerosis Pattern II Demyelinating Lesions

Project description:Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system with marked heterogeneity in several aspects including pathological processes. Four histopathological patterns of MS have been described. Pattern II is characterized by antibody and complement deposition. MS is considered a prototypic T cell-mediated disease, but until now the study of pathogenic T cells has encountered major challenges, most importantly the limited access of brain-infiltrating T cells. Here, we used next generation sequencing to identify clonally expanded T cells in demyelinating pattern II brain autopsy lesions and subsequently isolated these as T cell clones from autologous cerebrospinal fluid. The functional characterization shows that T cells releasing Th2 cytokines and able to provide B cell help dominate the T cell infiltrate in pattern II brain lesions. Our data provide the first functional evidence for a role of Th2/Tc2 cells in pattern II MS. Two stimulated CD4+ Th2 brain infiltrating T cell clones compared with stimulated circulaiting memory CD4+ T cells and two stimulated CD8+ T cell clones (one Tc1 and one Tc2) compared with each other.

2016-07-03 | E-GEOD-60914 | biostudies-arrayexpress

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Central Role of Th2 and Tc2 Lymphocytes in Multiple Sclerosis Pattern II Demyelinating Lesions

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Project description:Central Role of Th2 and Tc2 Lymphocytes in Multiple Sclerosis Pattern II Demyelinating Lesions

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Transcriptional changes in demyelinating canine distemper virus encephalitis

Project description:Canine distemper virus (CDV)-induced demyelinating leukoencephalitis (CDV-DL) in dogs is a translational animal model for human demyelinating diseases such as multiple sclerosis. The aim of this study was to perform an assumption-free microarray analysis of gene expression in different subgroups of CDV-DL as compared to normal controls. Dogs were classified into normal controls (group 1), acute CDV-DL lesions with CDV within the brain but without demyelination and inflammation (group 2), subacute lesions with demyelination but without inflammation (group 3), and subacute to chronic lesions with demyelination and inflammation (group 4).

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Pro-inflammatory activity following demyelinating injury is required for phagocytic function and oligodendrocyte formation

Project description:Remyelination can occur naturally in demyelinating lesions, but often fails in human demyelinating diseases such as multiple sclerosis (MS). The function of the innate immune system is essential for the regenerative response, but how exactly microglia and macrophages clear myelin debris after injury and tailor a specific regenerative response is unclear. Here, we asked whether pro-inflammatory microglial/macrophage activation is required for this process. We established a novel toxin-based spinal cord model of de- and remyelination in zebrafish and showed that pro-inflammatory nuclear factor κB (NF-κB) dependent activation occurs in phagocytes rapidly after myelin injury. We found that the pro-inflammatory response depends on myeloid differentiation primary response 88 (MyD88), the canonical adaptor for inflammatory signaling pathways downstream of toll-like receptors (TLRs). MyD88-deficient mice and zebrafish were impaired not only in the degradation of myelin debris, but also in initiating the generation of new oligodendrocytes for myelin repair. We identified reduced generation of tumor necrosis factor-α (TNF-α) in lesions of MyD88-deficient animals, a pro-inflammatory molecule that was able to induce the generation of new oligodendrocytes. Our study shows that pro-inflammatory phagocytic signaling is an evolutionary conserved mechanism necessary for degrading myelin debris, essential for inflammation resolution, and for initiating the secretion of pro-inflammatory myelin repair molecules.

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