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dc.contributor.authorCamacho, SA
dc.contributor.authorHeath, WR
dc.contributor.authorCarbone, FR
dc.contributor.authorSarvetnick, N
dc.contributor.authorLeBon, A
dc.contributor.authorKarlsson, L
dc.contributor.authorPeterson, PA
dc.contributor.authorWebb, SR
dc.date.available2014-05-21T19:24:06Z
dc.date.issued2001-06-01
dc.identifierpii: 88720
dc.identifier.citationCamacho, S. A., Heath, W. R., Carbone, F. R., Sarvetnick, N., LeBon, A., Karlsson, L., Peterson, P. A. & Webb, S. R. (2001). A key role for ICAM-I in generating effector cells mediating inflammatory responses. NATURE IMMUNOLOGY, 2 (6), pp.523-529. https://doi.org/10.1038/88720.
dc.identifier.issn1529-2908
dc.identifier.urihttp://hdl.handle.net/11343/26228
dc.descriptionC1 - Journal Articles Refereed
dc.description.abstractWe investigated how the accessory molecule interactions encountered during T cell priming influence T cell-mediated destruction of insulin-producing beta cells and lead to type 1 diabetes. T cell receptor (TCR)-transgenic CD4+ T cells were primed under controlled conditions in vitro before being adoptively transferred into transgenic recipients expressing membrane ovalbumin under the control of the rat insulin promoter (RIP-mOVA). During priming, antigen-presenting cell expression of B7-1 without intracellular adhesion molecule 1 (ICAM-1) led to the generation of effector cells that migrated to the pancreata of RIP-mOVA recipients but did not cause diabetes. In contrast, when T cells were primed with APCs expressing both B7-1 and ICAM-1, pronounced destruction of beta cells and a rapid onset of diabetes were observed. Pathogenicity was associated with T cell production of the macrophage-attracting chemokines CCL3 and CCL4. Thus, interactions of lymphocyte function-associated antigen 1 with ICAM-1 during priming induce both qualitative and quantitative alterations in T effector function and induce potentially autodestructive responses.
dc.formatapplication/pdf
dc.languageEnglish
dc.publisherNATURE PUBLISHING GROUP
dc.subjectCellular Immunology; Immune System and Allergy
dc.titleA key role for ICAM-I in generating effector cells mediating inflammatory responses
dc.typeJournal Article
dc.identifier.doi10.1038/88720
melbourne.peerreviewPeer Reviewed
melbourne.affiliationThe University of Melbourne
melbourne.affiliation.departmentMicrobiology And Immunology
melbourne.source.titleNATURE IMMUNOLOGY
melbourne.source.volume2
melbourne.source.issue6
melbourne.source.pages523-529
dc.research.coderfcd320202
dc.research.codeseo1998730102
melbourne.publicationid78595
melbourne.elementsid289159
melbourne.contributor.authorCarbone, Francis
melbourne.contributor.authorHeath, William
dc.identifier.eissn1529-2916
melbourne.accessrightsThis item is currently not available from this repository


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