About: Different Mechanisms of Inflammation Induced in Virus and Autoimmune-Mediated Models of Multiple Sclerosis in C57BL6 Mice

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About: Different Mechanisms of Inflammation Induced in Virus and Autoimmune-Mediated Models of Multiple Sclerosis in C57BL6 Mice Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Different Mechanisms of Inflammation Induced in Virus and Autoimmune-Mediated Models of Multiple Sclerosis in C57BL6 Mice
Creator	Das Sarma, Jayasri Kanaujia, Anurag Kishore, Abhinoy Nag, Soma Kenyon, Lawrence Shindler, Kenneth Rostami, A
Source	PMC
abstract	Multiple sclerosis (MS) is an inflammatory demyelinating disease of the human central nervous system (CNS). Neurotropic demyelinating strain of MHV (MHV-A59 or its isogenic recombinant strain RSA59) induces MS-like disease in mice mediated by microglia, along with a small population of T cells. The mechanism of demyelination is at least in part due to microglia-mediated myelin stripping, with some direct axonal injury. Immunization with myelin oligodendrocyte glycoprotein (MOG) induces experimental autoimmune encephalomyelitis (EAE), a mainly CD4(+) T-cell-mediated disease, although CD8(+) T cells may play a significant role in demyelination. It is possible that both autoimmune and nonimmune mechanisms such as direct viral toxicity may induce MS. Our study directly compares CNS pathology in autoimmune and viral-induced MS models. Mice with viral-induced and EAE demyelinating diseases demonstrated similar patterns and distributions of demyelination that accumulated over the course of the disease. However, significant differences in acute inflammation were noted. Inflammation was restricted mainly to white matter at all times in EAE, whereas inflammation initially largely involved gray matter in acute MHV-induced disease and then is subsequently localized only in white matter in the chronic disease phase. The presence of dual mechanisms of demyelination may be responsible for the failure of immunosuppression to promote long-term remission in many MS patients.
has issue date	2013-08-28(xsd:dateTime)
bibo:doi	10.1155/2013/589048
bibo:pmid	24083230
has license	cc-by
sha1sum (hex)	f292a5fa02dc7ce9ea268920cc8657f4e34360f9
schema:url	https://doi.org/10.1155/2013/589048
resource representing a document's title	Different Mechanisms of Inflammation Induced in Virus and Autoimmune-Mediated Models of Multiple Sclerosis in C57BL6 Mice
has PubMed Central identifier	PMC3780522
has PubMed identifier	24083230
schema:publication	Biomed Res Int
resource representing a document's body	covid:f292a5fa02dc7ce9ea268920cc8657f4e34360f9#body_text
is schema:about of	named entity 'inflammation' named entity 'study' named entity 'Our' named entity 'toxicity' named entity 'CD8' named entity 'disease' named entity 'disease' named entity 'direct' named entity 'disease' named entity 'MS-' named entity 'CD4' named entity 'MHV' named entity 'INDUCED' named entity 'INITIALLY' named entity 'PATHOLOGY' named entity 'T CELLS' named entity 'ACCUMULATED' named entity 'OUR' named entity 'AUTOIMMUNE' named entity 'INVOLVED' named entity 'COURSE' named entity 'VIRAL' named entity 'MECHANISMS' named entity 'PLAY' named entity 'T-CELL' named entity 'NOTED' named entity 'REMISSION' named entity 'WHITE MATTER' named entity 'MICROGLIA' named entity 'MYELIN' named entity 'AXONAL INJURY' named entity 'DEMYELINATING DISEASE' named entity 'POSSIBLE' named entity 'POPULATION' named entity 'MECHANISM' named entity 'EAE' named entity 'RESPONSIBLE' named entity 'RECOMBINANT' named entity 'MS.' named entity 'STRIPPING' named entity 'MYELIN OLIGODENDROCYTE GLYCOPROTEIN' named entity 'TIMES' named entity 'SMALL' named entity 'LARGELY' named entity 'MEDIATED' named entity 'DEMYELINATING DISEASES' named entity 'IMMUNOSUPPRESSION' named entity 'LIKE' named entity 'PROMOTE' named entity 'CENTRAL NERVOUS SYSTEM' named entity 'INFLAMMATION' named entity 'CNS' named entity 'STUDY' named entity 'MODELS' named entity 'A59' named entity 'DISEASE' covid:arg/f292a5fa02dc7ce9ea268920cc8657f4e34360f9 named entity 'FAILURE' named entity 'ITS' named entity 'LONG-TERM' named entity 'AUTOIMMUNE' named entity 'MICE' named entity 'DIFFERENT' named entity 'MODELS' named entity 'INDUCED' named entity 'INFLAMMATION' named entity 'TOXICITY' named entity 'RESTRICTED' named entity 'INDUCE' named entity 'ISOGENIC' named entity 'DUAL' named entity 'MECHANISMS' named entity 'MULTIPLE SCLEROSIS' named entity 'DUE TO' named entity 'CHRONIC DISEASE'

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