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The Journal of Immunology, Vol 158, Issue 1 5-8, Copyright © 1997 by American Association of Immunologists
CUTTING EDGE |
JW Maciaszek, NA Parada, WW Cruikshank, DM Center, H Kornfeld and GA Viglianti
The Program in Virology and Immunology, University of Massachusetts Medical Center, Worcester 01605, USA.
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.
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