Maciaszek, Joseph WalterParada, Nereida A.Cruikshank, William W.Center, David M.Kornfeld, HardyViglianti, Gregory A.2022-08-232022-08-231997-01-012008-11-05<p>J Immunol. 1997 Jan 1;158(1):5-8.</p>0022-1767 (Print)8977168https://hdl.handle.net/20.500.14038/34137IL-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.en-USJournal Articlehttps://escholarship.umassmed.edu/gsbs_sp/799661909gsbs_sp/799