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dc.contributor.authorRolph, Michael S.
dc.contributor.authorYoung, Timothy R.
dc.contributor.authorShum, Bennett O. V.
dc.contributor.authorGorgun, Cem Z.
dc.contributor.authorSchmitz-Peiffer, Carsten
dc.contributor.authorRamshaw, Ian A.
dc.contributor.authorHotamisligil, Gökhan S.
dc.contributor.authorMackay, Charles R.
dc.date.accessioned2017-05-03T16:02:14Z
dc.date.available2017-05-03T16:02:14Z
dc.date.issued2006
dc.date.modified2013-12-12T03:26:52Z
dc.identifier.issn1550-6606
dc.identifier.doi10.4049/jimmunol.177.11.7794
dc.identifier.urihttp://hdl.handle.net/10072/54898
dc.description.abstractThe fatty acid-binding protein (FABP) family consists of a number of conserved cytoplasmic proteins with roles in intracellular lipid transport, storage, and metabolism. Examination of a comprehensive leukocyte gene expression database revealed strong expression of the adipocyte FABP aP2 in human monocyte-derived dendritic cells (DCs). We isolated bone marrow-derived DC from aP2-deficient mice, and showed that expression of DC cytokines including IL-12 and TNF was significantly impaired in these cells. Degradation of I?Ba was also impaired in aP2-deficient DCs, indicative of reduced signaling through the I?B kinase-NF-?B pathway. The cytokine defect was selective because there was no effect on Ag uptake or expression of MHC class II, CD40, CD80, or CD86. In an MLR, aP2-deficient DCs stimulated markedly lower T cell proliferation and cytokine production than did wild-type DCs. Moreover, aP2-deficient mice immunized with keyhole limpet hemocyanin/CFA showed reduced production of IFN-? by restimulated draining lymph node cells, suggesting a similar defect in DC function in vivo. Similarly, infection of aP2-deficient mice with the natural mouse pathogen ectromelia virus resulted in substantially lower production of IFN-? by CD8+ T cells. Thus, FABP aP2 plays an important role in DC function and T cell priming, and provides an additional link between metabolic processes and the regulation of immune responses.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherAmerican Association of Immunologists
dc.publisher.placeUnited States
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom7794
dc.relation.ispartofpageto7801
dc.relation.ispartofissue11
dc.relation.ispartofjournalJournal of Immunology
dc.relation.ispartofvolume177
dc.rights.retentionY
dc.subject.fieldofresearchCellular Immunology
dc.subject.fieldofresearchImmunology
dc.subject.fieldofresearchcode110704
dc.subject.fieldofresearchcode1107
dc.titleRegulation of Dendritic Cell Function and T Cell Priming by the Fatty Acid-Binding Protein aP2
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.
gro.date.issued2006
gro.hasfulltextNo Full Text
gro.griffith.authorRolph, Michael S.


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