Literature DB >> 18075273

Positive and negative implications of tumor necrosis factor neutralization for the pathogenesis of multiple sclerosis.

E Taoufik1, V Tseveleki, M Euagelidou, M Emmanouil, A Voulgari-Kokota, S Haralambous, L Probert.   

Abstract

Multiple sclerosis (MS) is a progressive, presumably autoimmune, degenerative disease of the central nervous system (CNS). The mechanisms which trigger the disease are unknown, but the pathology of MS is caused by the host's own immune system, which invades the CNS and attacks the myelin sheath that protects and insulates the axons of the nerve cells. Although this inflammatory assault selectively destroys myelin, it is believed that the neurological deficits of MS are rather the consequence of damage to axons, which occurs secondary to inflammation. The inflammatory mediators are generally secreted by myelin-specific, CD4+ T cells, CD8+ T cells, macrophages and activated glial cells and include a large number of cytokines, chemokines and other proinflammatory proteins. Copyright (c) 2008 S. Karger AG, Basel.

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Year:  2008        PMID: 18075273     DOI: 10.1159/000109936

Source DB:  PubMed          Journal:  Neurodegener Dis        ISSN: 1660-2854            Impact factor:   2.977


  2 in total

1.  Genetic ablation of soluble tumor necrosis factor with preservation of membrane tumor necrosis factor is associated with neuroprotection after focal cerebral ischemia.

Authors:  Pernille M Madsen; Bettina H Clausen; Matilda Degn; Stine Thyssen; Lotte K Kristensen; Martina Svensson; Nicholas Ditzel; Bente Finsen; Tomas Deierborg; Roberta Brambilla; Kate L Lambertsen
Journal:  J Cereb Blood Flow Metab       Date:  2015-10-19       Impact factor: 6.200

2.  Cerebral ischemia-induced angiogenesis is dependent on tumor necrosis factor receptor 1-mediated upregulation of α5β1 and αVβ3 integrins.

Authors:  Heng Huang; Qijuan Huang; Fuxin Wang; Richard Milner; Longxuan Li
Journal:  J Neuroinflammation       Date:  2016-09-01       Impact factor: 8.322

  2 in total

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