Cytokine production by dendritic cells genetically engineered to express IL-4: induction of Th2 responses and differential regulation of IL-12 and IL-23 synthesis
dc.contributor.author | Morita, Yoshitaka | en_US |
dc.contributor.author | Gupta, Raj | en_US |
dc.contributor.author | Seidl, Kelly M. | en_US |
dc.contributor.author | McDonagh, Kevin T. | en_US |
dc.contributor.author | Fox, David A. | en_US |
dc.date.accessioned | 2006-09-20T15:02:45Z | |
dc.date.available | 2006-09-20T15:02:45Z | |
dc.date.issued | 2005-07 | en_US |
dc.identifier.citation | Morita, Yoshitaka; Gupta, Raj; Seidl, Kelly M.; McDonagh, Kevin T.; Fox, David A. (2005)."Cytokine production by dendritic cells genetically engineered to express IL-4: induction of Th2 responses and differential regulation of IL-12 and IL-23 synthesis." The Journal of Gene Medicine 7(7): 869-877. <http://hdl.handle.net/2027.42/48697> | en_US |
dc.identifier.issn | 1099-498X | en_US |
dc.identifier.issn | 1521-2254 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/48697 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=15712252&dopt=citation | en_US |
dc.description.abstract | Dendritic cells (DCs) retrovirally transduced with IL-4 have recently been shown to inhibit murine collagen-induced arthritis and associated Th1 immune responses in vivo , but the mechanisms that underly these effects are not yet understood. In this report we demonstrate that IL-4-transduced DCs loaded with antigen led to lower T cell production of IFN-Γ, increased production of IL-4, and an attenuated, delayed type hypersensitivity response. We hypothesized that the ability of such DCs to regulate the Th1 immune response in vivo depends in part on their capacity to produce IL-12 and IL-23. Quantitative mRNA analysis revealed that IL-4-transduced DCs stimulated with CD40 ligand expressed higher levels of IL-12p35 mRNA, but lower levels of mRNA for IL-23p19 and the common subunit p40 found in both IL-12 and IL-23, compared with control DCs. These results, which indicate that expression of the IL-12 and IL-23 subunits is differentially regulated in IL-4-transduced DCs, were confirmed by ELISA of the IL-12 and IL-23 heterodimers. Thus, therapeutic suppression of Th1 -mediated autoimmunity (as recently shown in murine collagen-induced arthritis) and induction of Th2 responses in vivo by IL-4-transduced DCs occurs despite their potential to produce increased levels of IL-12, but could reflect, in part, decreased production of IL-23. Copyright © 2005 John Wiley & Sons, Ltd. | en_US |
dc.format.extent | 179182 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | John Wiley & Sons, Ltd. | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Genetics | en_US |
dc.title | Cytokine production by dendritic cells genetically engineered to express IL-4: induction of Th2 responses and differential regulation of IL-12 and IL-23 synthesis | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbsecondlevel | Genetics | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Division of Rheumatology, Department of Internal Medicine, and Rheumatic Disease Core Center, University of Michigan, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationum | Division of Rheumatology, Department of Internal Medicine, and Rheumatic Disease Core Center, University of Michigan, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationum | Division of Hematology and Oncology, Department of Internal Medicine, and Rheumatic Disease Core Center, University of Michigan, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationum | Division of Rheumatology, Department of Internal Medicine, and Rheumatic Disease Core Center, University of Michigan, Ann Arbor, MI, USA ; Division of Rheumatology, University of Michigan, 5520 MSRB I, 1150 W. Medical Center Dr., Ann Arbor, MI 48109, USA. | en_US |
dc.contributor.affiliationother | Division of Nephrology and Rheumatology, Department of Internal Medicine, Kawasaki Medical School, Kurashiki, Japan | en_US |
dc.identifier.pmid | 15712252 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/48697/1/730_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/jgm.730 | en_US |
dc.identifier.source | The Journal of Gene Medicine | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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