Linked Life Data

3121256

Source:http://linkedlifedata.com/resource/pubmed/id/3121256

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1988-2-10
pubmed:abstractText
CIA is a unique experimental model of disease, which may be particularly relevant to the study of RA, since it represents a true autoimmune reaction against a major joint component. Since it represents a model of the association of MHC genes and disease, it has a broad relevance to the study of disease, particularly the contribution of class II MHC genes to autoimmunity. This disease model has been demonstrated in three species, and a marked influence of immunogenetic control is apparent. Native type II collagen is a large protein with a genetically conserved structure, giving rise to a number of cross-reactive antigen epitopes between species. Susceptibility to CIA correlates with an Ir directed against certain epitopes, and this autoimmune response appears to be controlled by MHC-linked genes. In the mouse, susceptibility has been specifically associated with variations in the I-A beta chain. The immunogenetic control may be effected through the T-cell recognition of the collagen molecule, resulting in antibodies and reactive cells with a specificity for native autologous type II collagen. Although the specificity of the anti-type II collagen response is the critical element in the generation of the autoimmune reaction, production of a high level of antibody is important, as well as a complement-fixing isotype. Cell-mediated immunity to type II collagen contributes to the disease chronicity, either through the generation of inappropriate T help, or a suppressor defect, and the production of factors. However, the precise sequence of events, from antigen recognition to joint damage, has yet to be elucidated fully. Some aspects of this experimental model bear a striking resemblence to RA. Hopefully, this experimental model will provide valuable insights into the significance of collagen autoimmunity and the contribution of class II genes to the pathology of arthritic disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1040-8401
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-22
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Immunogenetics of collagen-induced arthritis.
pubmed:affiliation
Department of Immunology, Ayerst Laboratories Research, Inc. Princeton, New Jersey.
pubmed:publicationType
Journal Article, Review