Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1983-10-28
pubmed:abstractText
It is hypothesized that the underlying immunoregulatory dysfunction in systemic lupus erythematosus (SLE) is altered recognition by T cells of self class II major histocompatibility antigens (Ia). The resultant cellular autoreactivity would directly cause certain of the immunopathological manifestations of SLE. The perception by T cells of self non-MHC antigens in the context of altered Ia on antigen presenting cells would also stimulate specific help for autoantibody production. Autoimmunity induced by the graft-versus-host reaction is an experimental model that illustrates this potential mechanism (A. G. Rolink, S. T. Pals, and E. Gleichmann, J. Exp. Med. 157, 755, 1983; R. A. Eisenberg, S. Y. Craven, and P. L. Cohen, Arth. Rheum. 26, S19, 1983).
pubmed:grant
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
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
Class II major histocompatibility antigens and the etiology of systemic lupus erythematosus.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't