dc.contributor.author | Rolph, Michael S. | |
dc.contributor.author | Young, Timothy R. | |
dc.contributor.author | Shum, Bennett O. V. | |
dc.contributor.author | Gorgun, Cem Z. | |
dc.contributor.author | Schmitz-Peiffer, Carsten | |
dc.contributor.author | Ramshaw, Ian A. | |
dc.contributor.author | Hotamisligil, Gökhan S. | |
dc.contributor.author | Mackay, Charles R. | |
dc.date.accessioned | 2017-05-03T16:02:14Z | |
dc.date.available | 2017-05-03T16:02:14Z | |
dc.date.issued | 2006 | |
dc.date.modified | 2013-12-12T03:26:52Z | |
dc.identifier.issn | 1550-6606 | |
dc.identifier.doi | 10.4049/jimmunol.177.11.7794 | |
dc.identifier.uri | http://hdl.handle.net/10072/54898 | |
dc.description.abstract | The 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.peerreviewed | Yes | |
dc.description.publicationstatus | Yes | |
dc.language | English | |
dc.language.iso | eng | |
dc.publisher | American Association of Immunologists | |
dc.publisher.place | United States | |
dc.relation.ispartofstudentpublication | N | |
dc.relation.ispartofpagefrom | 7794 | |
dc.relation.ispartofpageto | 7801 | |
dc.relation.ispartofissue | 11 | |
dc.relation.ispartofjournal | Journal of Immunology | |
dc.relation.ispartofvolume | 177 | |
dc.rights.retention | Y | |
dc.subject.fieldofresearch | Cellular Immunology | |
dc.subject.fieldofresearch | Immunology | |
dc.subject.fieldofresearchcode | 110704 | |
dc.subject.fieldofresearchcode | 1107 | |
dc.title | Regulation of Dendritic Cell Function and T Cell Priming by the Fatty Acid-Binding Protein aP2 | |
dc.type | Journal article | |
dc.type.description | C1 - Articles | |
dc.type.code | C - Journal Articles | |
gro.rights.copyright | Self-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.issued | 2006 | |
gro.hasfulltext | No Full Text | |
gro.griffith.author | Rolph, Michael S. | |