Linked Life Data

15546398

Source:http://linkedlifedata.com/resource/pubmed/id/15546398

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2004-11-19
pubmed:abstractText
Cytokine-driven inflammation and tissue destruction is a common theme of chronic inflammatory diseases such as rheumatoid arthritis, Crohn's disease, ulcerative colitis, psoriasis, chronic obstructive pulmonary disease, and atherosclerosis. Research over the last two decades demonstrated the importance of cytokines that are not only expressed chronically but also are capable of signaling at sites of chronic inflammation. Cytokines thus regulate major pathological processes that include inflammation, angiogenesis, tissue remodeling, and fibrosis. This research led to the identification of key cytokines involved in these processes, two of which, tumor necrosis factor-alpha and interleukin-1, have also been successfully targeted in the clinic. However, what triggers and maintains cytokine gene expression in chronic inflammation remains a mystery. In this article, we review current progress in the understanding of cytokine-driven inflammation and discuss current evidence implicating Toll-like receptors (TLRs), recently identified as the receptors recognizing self versus non-self molecular patterns, in the regulation of cytokine-driven inflammation. Whether targeting TLRs and their downstream signaling pathway will prove to be a successful approach for the treatment of these devastating diseases remains to be determined.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0105-2896
pubmed:author
pubmed:issnType
Print
pubmed:volume
202
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
250-65
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Is targeting Toll-like receptors and their signaling pathway a useful therapeutic approach to modulating cytokine-driven inflammation?
pubmed:affiliation
Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College of Science, Technology and Medicine, London, UK.
pubmed:publicationType
Journal Article, Review