Fractalkine in rheumatoid arthritis: a review to date.

Hdl Handle:
http://hdl.handle.net/10147/209018
Title:
Fractalkine in rheumatoid arthritis: a review to date.
Authors:
Murphy, G; Caplice, N; Molloy, M
Affiliation:
Department of Rheumatology, Cork University Hospital, Wilton, Cork, Ireland., grainne.murphy@ucc.ie
Citation:
Rheumatology (Oxford). 2008 Oct;47(10):1446-51. Epub 2008 May 21.
Journal:
Rheumatology (Oxford, England)
Issue Date:
3-Feb-2012
URI:
http://hdl.handle.net/10147/209018
DOI:
10.1093/rheumatology/ken197
PubMed ID:
18495821
Abstract:
Rheumatoid arthritis (RA) is characterized by the expansion of the synovium, with infiltration of pro-inflammatory cells, neovascularization and an abundance of pro-inflammatory cytokines resulting in tissue destruction and bone erosion. Fractalkine (FKN), a recently described chemokine, possesses chemotactic, angiogenic and adhesive functions that associates it with all of these destructive processes. In this review, we describe the research to date, which implicates FKN and its receptor in the pathogenesis of RA and propose that this molecule may represent a future therapeutic target for RA.
Language:
eng
MeSH:
Antirheumatic Agents/therapeutic use; Arthritis, Rheumatoid/drug therapy/*physiopathology; Chemokine CX3CL1/antagonists & inhibitors/*physiology; Chemotaxis, Leukocyte; Humans; Neovascularization, Pathologic/physiopathology; Synovial Membrane/blood supply/pathology
ISSN:
1462-0332 (Electronic); 1462-0324 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorMurphy, Gen_GB
dc.contributor.authorCaplice, Nen_GB
dc.contributor.authorMolloy, Men_GB
dc.date.accessioned2012-02-03T15:10:03Z-
dc.date.available2012-02-03T15:10:03Z-
dc.date.issued2012-02-03T15:10:03Z-
dc.identifier.citationRheumatology (Oxford). 2008 Oct;47(10):1446-51. Epub 2008 May 21.en_GB
dc.identifier.issn1462-0332 (Electronic)en_GB
dc.identifier.issn1462-0324 (Linking)en_GB
dc.identifier.pmid18495821en_GB
dc.identifier.doi10.1093/rheumatology/ken197en_GB
dc.identifier.urihttp://hdl.handle.net/10147/209018-
dc.description.abstractRheumatoid arthritis (RA) is characterized by the expansion of the synovium, with infiltration of pro-inflammatory cells, neovascularization and an abundance of pro-inflammatory cytokines resulting in tissue destruction and bone erosion. Fractalkine (FKN), a recently described chemokine, possesses chemotactic, angiogenic and adhesive functions that associates it with all of these destructive processes. In this review, we describe the research to date, which implicates FKN and its receptor in the pathogenesis of RA and propose that this molecule may represent a future therapeutic target for RA.en_GB
dc.language.isoengen_GB
dc.subject.meshAntirheumatic Agents/therapeutic useen_GB
dc.subject.meshArthritis, Rheumatoid/drug therapy/*physiopathologyen_GB
dc.subject.meshChemokine CX3CL1/antagonists & inhibitors/*physiologyen_GB
dc.subject.meshChemotaxis, Leukocyteen_GB
dc.subject.meshHumansen_GB
dc.subject.meshNeovascularization, Pathologic/physiopathologyen_GB
dc.subject.meshSynovial Membrane/blood supply/pathologyen_GB
dc.titleFractalkine in rheumatoid arthritis: a review to date.en_GB
dc.contributor.departmentDepartment of Rheumatology, Cork University Hospital, Wilton, Cork, Ireland., grainne.murphy@ucc.ieen_GB
dc.identifier.journalRheumatology (Oxford, England)en_GB
dc.description.provinceMunster-

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