Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2002-7-2
pubmed:abstractText
Rheumatoid arthritis (RA) is a chronic inflammatory synovitis that is dominated by the presence of macrophages, lymphocytes and synovial fibroblasts, which leads to the destruction of bone and cartilage. The effectiveness of therapies that are directed against tumour-necrosis factor and interleukin-1 has identified macrophages as a crucial target for therapeutic intervention. However, not all patients respond to these therapies, and the benefits of this form of treatment are short lived. Recent work indicates that the insufficient apoptosis of inflammatory cells in the RA joint might contribute to pathogenesis. In this article, I characterize the mechanisms that prevent the apoptosis of chronic inflammatory cells in the RA joint, to identify potential new targets for the treatment of RA.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1474-1733
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
527-35
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Apoptosis as a therapeutic tool in rheumatoid arthritis.
pubmed:affiliation
Division of Rheumatology, Northwestern University, The Feinberg School of Medicine, Ward 3-315, 303 East Chicago Avenue, Chicago, Illinois 60611, USA. rmp158@northwestern.edu
pubmed:publicationType
Journal Article, Review