Linked Life Data

7554482

Source:http://linkedlifedata.com/resource/pubmed/id/7554482

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-10-25
pubmed:abstractText
The cause of multiple sclerosis (MS) is unknown, but the pathology is consistent with an immunological etiology. Studies conducted with the animal model of MS, experimental autoimmune encephalomyelitis (EAE), have provided insight into how the immune system can provoke an immunopathological response characteristic of that seen in MS. The use of inbred rats and mice for studies of EAE has been especially rewarding with respect to the identification of the epitopes of encephalitogenic antigens responsible for the induction of this autoimmune disease and in elucidating the effector mechanism underlying EAE. Moreover, it has also been possible to ascertain how EAE can be regulated, leading to therapeutic modalities which have been applied in clinical studies of MS patients. This review briefly summarizes studies of EAE in rodents, drawing comparisons with immunological findings reported in patients with MS. It is clear that important lessons can be learned from the detailed investigation of animal models that may be applicable to human immunological disorders.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0090-1229
pubmed:author
pubmed:issnType
Print
pubmed:volume
77
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4-13
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Experimental autoimmune encephalomyelitis in rodents as a model for human demyelinating disease.
pubmed:affiliation
Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't