Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autoreactive T cells specific for myelin basic protein (MBP), a major component of central nervous system (CNS) protein, are frequently found in blood and cerebrospinal fluid of patients with postinfectious encephalomyelitis. This autoimmune syndrome is a CNS complication after infections with a number of different enveloped viruses, e.g. mumps, measles, rubella, influenza and varicella. However, the pathophysiological mechanism leading to this breaking of natural self tolerance in the course of viral infection remains an enigma. A long-lasting hypothesis has suggested that incorporation of cellular (self) proteins into the envelope of budding viruses might be a possible mechanism leading to autosensitization. In a model study we demonstrate here that vesicular stomatitis virus (VSV), grown in myelin protein-expressing cell cultures, is highly efficient in triggering T cell responses to MBP in vitro and can prime autoreactive T cell immune responses in vivo. On the basis of these findings, we suggest that incorporation of CNS membrane components into the viral envelope and subsequent priming of self-reactive immune responses might be the common pathogenic mechanism underlying the postinfectious encephalomyelitis syndrome.
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PMID:Autoimmunity caused by host cell protein-containing viruses. 753 Dec 73

The exact diagnosis of demyelinating diseases is an enigma even in the best neurological centres. In the present study, the potential role of differential CSF proteins has been critically evaluated in differentiating multiple sclerosis (MS) and acute disseminated encephalomyelitis (ADEM). Cellulose acetate electrophoresis was carried out on CSF and serum samples of 14 MS patients, 23 ADEM patients and 30 controls. There was no statistically significant difference between serum electrophoresis of controls and MS patients. However, in case of CSF electrophoresis there was a statistically significant decrease in beta-1 fraction in 92.2% of MS patients (p=0.01). A comparison between serum electrophoresis of controls and ADEM patients indicated a statistically significant decrease in serum albumin in 87% patients and an increase of alpha-2 globulin in 73.9%. There was no statistically significant difference between CSF electrophoresis of controls and ADEM patients except for the prealbumin fraction which was raised in 60.9% of patients. No statistically significant difference was seen between the serum electrophoresis of ADEM and MS patients. However, on comparing CSF electrophoresis, it was seen that beta-1 fraction was significantly higher in ADEM patients (p<0.05). The predictive value of beta-1 fraction in differentiating MS and ADEM was then evaluated. The negative predictive value was 100% indicating that all samples with a beta-1 fraction of>6.5% cannot be diagnosed as MS. The significant decrease in beta-1 fraction in MS patients may prove to be an early indicator in differentiating between MS and ADEM patients.
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PMID:CSF beta-1 Globulin--a potential marker in differentiating multiple sclerosis and acute disseminated encephalomyelitis: a preliminary study. 1196 Jan 50

Multiple sclerosis (MScl) is defined by central nervous system (CNS) inflammation, demyelination and axonal damage. Some of the disease mechanisms are known but the cause of this complex disorder stays an enigma. Experimental autoimmune encephalomyelitis (EAE) is an animal model mimicking many aspects of MScl. This review aims to provide an overview over proteomic biomarker studies in the EAE model emphasizing the translational aspects with respect to MScl in humans.
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PMID:The experimental autoimmune encephalomyelitis model for proteomic biomarker studies: from rat to human. 2133 41

Women are more susceptible to multiple sclerosis (MS) and have more robust immune responses than men. However, men with MS tend to demonstrate a more progressive disease course than women, suggesting a disconnect between the severity of an immune attack and the CNS response to a given immune attack. We have previously shown in an MS model, experimental autoimmune encephalomyelitis, that autoantigen-sensitized XX lymph node cells, compared with XY, are more encephalitogenic. These studies demonstrated an effect of sex chromosomes in the induction of immune responses, but did not address a potential role of sex chromosomes in the CNS response to immune-mediated injury. Here, we examined this possibility using XX versus XY bone marrow chimeras reconstituted with a common immune system of one sex chromosomal type. We found that experimental autoimmune encephalomyelitis mice with an XY sex chromosome complement in the CNS, compared with XX, demonstrated greater clinical disease severity with more neuropathology in the spinal cord, cerebellum, and cerebral cortex. A candidate gene on the X chromosome, toll-like receptor 7, was then examined. Toll-like receptor 7 expression in cortical neurons was higher in mice with XY compared with mice with XX CNS, consistent with the known neurodegenerative role for toll-like receptor 7 in neurons. These results suggest that sex chromosome effects on neurodegeneration in the CNS run counter to effects on immune responses, and may bear relevance to the clinical enigma of greater MS susceptibility in women but faster disability progression in men. This is a demonstration of a direct effect of sex chromosome complement on neurodegeneration in a neurological disease.
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PMID:XY sex chromosome complement, compared with XX, in the CNS confers greater neurodegeneration during experimental autoimmune encephalomyelitis. 2455 Mar 11