Linked Life Data

1839881

Source:http://linkedlifedata.com/resource/pubmed/id/1839881

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1992-6-12
pubmed:abstractText
The role of classical pathway complement components in systemic lupus erythematosus (SLE) is reviewed. Their importance in maintaining immune complexes (IC) in soluble form and in enhancing clearance of IC through binding to red cell CR1 is such that deficiency, complete or partial, of these components or some of their controlling enzymes can lead to IC mediated disease like SLE. C2 and C4 are encoded within the class III region of the major histocompatibility complex (MHC). There are certain well described associations between class II MHC genes and the occurrence of SLE and the relative importance of the two sets of gene products and their potential interactions are discussed. Complement C4 plays a role in drug induced lupus as many of the lupus associated drugs bind to C4 and interfere with its protective functions. Classical genetic studies provide clear evidence that non MHC genes are important in the aetiopathogenesis of SLE. Non MHC encoded complement deficiencies and functional deficits may well represent some of these other genetic factors and is clearly a fertile area for future research.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0891-6934
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
61-6
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
The role of complement in the aetiopathogenesis of systemic lupus erythematosus.
pubmed:affiliation
Department of Clinical Immunology, Royal Prince Alfred Hospital, NSW, Australia.
pubmed:publicationType
Journal Article, Review