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dc.contributor.authorMcQualter, JL
dc.contributor.authorDarwiche, R
dc.contributor.authorEwing, C
dc.contributor.authorOnuki, M
dc.contributor.authorKay, TW
dc.contributor.authorHamilton, JA
dc.contributor.authorReid, HH
dc.contributor.authorBernard, CCA
dc.date.available2014-05-21T19:30:31Z
dc.date.issued2001-10-01
dc.identifierhttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000171671900002&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=d4d813f4571fa7d6246bdc0dfeca3a1c
dc.identifier.citationMcQualter, J. L., Darwiche, R., Ewing, C., Onuki, M., Kay, T. W., Hamilton, J. A., Reid, H. H. & Bernard, C. C. A. (2001). Granulocyte macrophage colony-stimulating factor: A new putative therapeutic target in multiple sclerosis. JOURNAL OF EXPERIMENTAL MEDICINE, 194 (7), pp.873-881. https://doi.org/10.1084/jem.194.7.873.
dc.identifier.issn0022-1007
dc.identifier.urihttp://hdl.handle.net/11343/26385
dc.descriptionC1 - Journal Articles Refereed
dc.description.abstractExperimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, can be induced by immunization with a number of myelin antigens. In particular, myelin oligodendrocyte glycoprotein, a central nervous system (CNS)-specific antigen expressed on the myelin surface, is able to induce a paralytic MS-like disease with extensive CNS inflammation and demyelination in several strains of animals. Although not well understood, the egress of immune cells into the CNS in EAE is governed by a complex interplay between pro and antiinflammatory cytokines and chemokines. The hematopoietic growth factor, granulocyte macrophage colony-stimulating factor (GM-CSF), is considered to play a central role in maintaining chronic inflammation. The present study was designed to investigate the previously unexplored role of GM-CSF in autoimmune-mediated demyelination. GM-CSF(-/)- mice are resistant to EAE, display decreased antigen-specific proliferation of splenocytes, and fail to sustain immune cell infiltrates in the CNS, thus revealing key activities for GM-CSF in the development of inflammatory demyelinating lesions and control of migration and/or proliferation of leukocytes within the CNS. These results hold implications for the pathogenesis of inflammatory and demyelinating diseases and may provide the basis for more effective therapies for inflammatory diseases, and more specifically for multiple sclerosis.
dc.formatapplication/pdf
dc.languageEnglish
dc.publisherROCKEFELLER UNIV PRESS
dc.subjectNeurology and Neuromuscular Diseases; Nervous System and Disorders
dc.titleGranulocyte macrophage colony-stimulating factor: A new putative therapeutic target in multiple sclerosis
dc.typeJournal Article
dc.identifier.doi10.1084/jem.194.7.873
melbourne.peerreviewPeer Reviewed
melbourne.affiliationThe University of Melbourne
melbourne.affiliation.departmentMedicine - Royal Melbourne And Western Hospitals
melbourne.source.titleJOURNAL OF EXPERIMENTAL MEDICINE
melbourne.source.volume194
melbourne.source.issue7
melbourne.source.pages873-881
dc.rights.licenseCC BY-NC-SA
melbourne.publicationid399
melbourne.elementsid246527
melbourne.openaccess.pmchttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193476
melbourne.contributor.authorKay, Thomas
melbourne.contributor.authorHamilton, John
dc.identifier.eissn1540-9538
melbourne.accessrightsAccess this item via the Open Access location


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