Linked Life Data

18490410

Source:http://linkedlifedata.com/resource/pubmed/id/18490410

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-5-20
pubmed:abstractText
Systemic lupus erythematosus (SLE) is a prototype inflammatory autoimmune disease resulting from autoimmune responses against nuclear autoantigens. During apoptosis many lupus autoantigens congregate inside the cells and are susceptible to modifications. Modified nuclear constituents are considered foreign and dangerous. Therefore, apoptotic cells have to has to be efficiently removed to avoid the accumulation of apoptotic debris and the subsequently development of autoimmune responses. Hence, apoptosis and clearance of apoptotic cells/material are considered key processes in the aetiology of SLE. Clearance deficiencies may account for the development of autoimmunity by inducing a loss of tolerance in lymphoid tissues. Furthermore, phagocytosis of apoptotic cells may lead to a pro-inflammatory response in the presence of autoantibodies. This may sustain inflammatory conditions and the pathology found in overt lupus.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0961-2033
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
371-5
pubmed:dateRevised
2011-3-11
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Apoptosis in the pathogenesis of systemic lupus erythematosus.
pubmed:affiliation
Department of Internal Medicine 3, Institute for Clinical Immunology, Friedrich-Alexander-University of Erlangen-Nuremberg, Erlangen, Germany.
pubmed:publicationType
Journal Article, Review