Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
1999-12-14
pubmed:abstractText
The conventional paradigm to explain systemic lupus erythematosus (SLE) is that disease results from tissue deposition of pathogenic autoantibodies and immune complexes, secondary to activation of autoreactive B cells in the context of help from alphabeta T cells. Recent work in murine lupus has confirmed this notion and demonstrated that autoantigen-specific alphabeta T cells are absolutely required for full penetrance of disease, with such autoreactive alphabeta T cells, even in Fas-intact mice, likely arising from defects in peripheral tolerance. These studies have also revealed a network of regulation that also involves nonclassical pathogenic and downregulatory alphabeta and gammadelta T cells, suggesting that the lupus immune system involves more complex interactions than the conventional paradigm suggests.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0257-277X
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
245-57
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Autoreactive T cells in murine lupus: origins and roles in autoantibody production.
pubmed:affiliation
Department of Medicine, Yale University School of Medicine, New Haven, CT 06520-8031, USA. joseph.craft@yale.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't