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IL-16 represses HIV-1 promoter activity

dc.contributor.authorMaciaszek, Joseph Walter
dc.contributor.authorParada, Nereida A.
dc.contributor.authorCruikshank, William W.
dc.contributor.authorCenter, David M.
dc.contributor.authorKornfeld, Hardy
dc.contributor.authorViglianti, Gregory A.
dc.date2022-08-11T08:09:01.000
dc.date.accessioned2022-08-23T16:15:38Z
dc.date.available2022-08-23T16:15:38Z
dc.date.issued1997-01-01
dc.date.submitted2008-11-05
dc.identifier.citation<p>J Immunol. 1997 Jan 1;158(1):5-8.</p>
dc.identifier.issn0022-1767 (Print)
dc.identifier.pmid8977168
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34137
dc.description.abstractIL-16 is produced by CD8+ lymphocytes and has been reported to inhibit HIV-1 and SIV replication in infected PBMCs. CD4 serves as a receptor for the secreted form of IL-16, and IL-16 binding to CD4 induces signal transduction, which affects the activation state of the cell. We hypothesized, therefore, that the effect of IL-16 on HIV-1 replication might occur at the level of virus expression. In transient transfection studies with HIV-1 LTR-reporter gene constructs we found that pretreatment of CD4+ lymphoid cells with recombinant IL-16 repressed HIV-1 promoter activity up to 60-fold, preventing both PMA and Tat activation. This effect of IL-16 required sequences contained within the core enhancer, but was not simply due to the down-regulation of transcription factors binding to this element.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8977168&dopt=Abstract">Link to article in PubMed</a></p>
dc.relation.urlhttp://www.jimmunol.org/content/158/1/5
dc.subjectDown-Regulation; Gene Products, tat; HIV Long Terminal Repeat; HIV-1; Humans; Interleukin-16; NF-kappa B; Virus Activation; tat Gene Products, Human Immunodeficiency Virus
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleIL-16 represses HIV-1 promoter activity
dc.typeJournal Article
dc.source.journaltitleJournal of immunology (Baltimore, Md. : 1950)
dc.source.volume158
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/799
dc.identifier.contextkey661909
html.description.abstract<p>IL-16 is produced by CD8+ lymphocytes and has been reported to inhibit HIV-1 and SIV replication in infected PBMCs. CD4 serves as a receptor for the secreted form of IL-16, and IL-16 binding to CD4 induces signal transduction, which affects the activation state of the cell. We hypothesized, therefore, that the effect of IL-16 on HIV-1 replication might occur at the level of virus expression. In transient transfection studies with HIV-1 LTR-reporter gene constructs we found that pretreatment of CD4+ lymphoid cells with recombinant IL-16 repressed HIV-1 promoter activity up to 60-fold, preventing both PMA and Tat activation. This effect of IL-16 required sequences contained within the core enhancer, but was not simply due to the down-regulation of transcription factors binding to this element.</p>
dc.identifier.submissionpathgsbs_sp/799
dc.contributor.departmentMedicine
dc.contributor.departmentMorningside Graduate School of Biomedical Sciences
dc.source.pages5-8
dc.contributor.studentJoseph Walter Maciaszek
dc.description.thesisprogramImmunology and Virology


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