Linked Life Data

10384097

Source:http://linkedlifedata.com/resource/pubmed/id/10384097

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-7-15
pubmed:abstractText
Experimental autoimmune encephalomyelitis (EAE) induced by active immunization with the myelin oligodendrocyte glycoprotein (MOG) is an Ab-mediated, T cell-dependent autoimmune disease that replicates the inflammatory demyelinating pathology of multiple sclerosis. We report that disease susceptibility and severity are determined by MHC and MHC-linked effects on the MOG-specific B cell response that mediate severe clinical EAE in the EAE-resistant Brown Norway (BN) rat. Immunization with the extracellular domain of MOG in CFA induced fulminant clinical disease associated with widespread demyelination and with an inflammatory infiltrate containing large numbers of polymorphonuclear cells and eosinophils within 10 days of immunization. To analyze the effects of the MHC (RT1 system) we compared BN (RT1 n) rats with Lewis (LEW) (RT1 l) and two reciprocal MHC congenic strains, LEW.1N (RT1n) and BN.1L (RT1 l). This comparison revealed that disease severity and clinical course were strongly influenced by the MHC haplotype that modulated the pathogenic MOG-specific autoantibody response. The intra-MHC recombinant congenic strain LEW.1R38 demonstrated that gene loci located both within the centromeric segment of the MHC containing classical class I and class II genes and within the telomeric RT1.M region containing the MOG gene are involved in determining Ab production and disease susceptibility. This study indicates that the current T cell-centered interpretation of MHC-mediated effects on disease susceptibility must be reassessed in multiple sclerosis and other autoimmune diseases in which autoantibody is involved in disease pathogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
40-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:10384097-Adoptive Transfer, pubmed-meshheading:10384097-Animals, pubmed-meshheading:10384097-Animals, Congenic, pubmed-meshheading:10384097-Antigens, Surface, pubmed-meshheading:10384097-Autoantibodies, pubmed-meshheading:10384097-B-Lymphocytes, pubmed-meshheading:10384097-Disease Susceptibility, pubmed-meshheading:10384097-Encephalomyelitis, Autoimmune, Experimental, pubmed-meshheading:10384097-Haplotypes, pubmed-meshheading:10384097-Immunity, Innate, pubmed-meshheading:10384097-Major Histocompatibility Complex, pubmed-meshheading:10384097-Myelin Proteins, pubmed-meshheading:10384097-Myelin-Associated Glycoprotein, pubmed-meshheading:10384097-Oligodendroglia, pubmed-meshheading:10384097-Rats, pubmed-meshheading:10384097-Rats, Inbred BN, pubmed-meshheading:10384097-Rats, Inbred Lew, pubmed-meshheading:10384097-Species Specificity, pubmed-meshheading:10384097-T-Lymphocytes
pubmed:year
1999
pubmed:articleTitle
Myelin oligodendrocyte glycoprotein induces experimental autoimmune encephalomyelitis in the "resistant" Brown Norway rat: disease susceptibility is determined by MHC and MHC-linked effects on the B cell response.
pubmed:affiliation
Department of Neuroimmunology, Max-Planck Institute for Neurobiology, Martinsried, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't