Linked Life Data

14531953

Source:http://linkedlifedata.com/resource/pubmed/id/14531953

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-10-8
pubmed:abstractText
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by B cell hyperactivity in association with autoantibodies, most prominently those directed to components of the cell nucleus. The source of the antigens that drive B cell responses in SLE is unknown, although recent studies suggest mechanisms by which the self-antigens become immunogenic and stimulate responses. Among these mechanisms, abnormalities in the generation of apoptotic cells or their clearance may increase the availability of nuclear antigens to drive responses. In addition, autoantibody crossreactivity may promote induction of responses to disparate antigens, foreign and self, and enable a single autoantibody to cause disease by crossreactive binding. In addition to reflecting increased exposure to self-antigen, autoantibody responses in SLE may result from abnormalities in B cell signaling and regulation by cytokines. New approaches to therapy aim to abrogate autoantibody production by targeting specific steps in B cell activation, including blockade of T cell costimulation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1523-3774
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
264-9
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
B lymphocytes and systemic lupus erythematosus.
pubmed:affiliation
Division of Rheumatology, Department of Medicine, Duke University Medical Center, 151G Durham VA Medical Center, 508 Fulton Street, Durham, NC 27705, USA.
pubmed:publicationType
Journal Article, Review