科研之友
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摘要
Objective: To explore whether expression of dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) and reactivation of human immunodeficiency virus type 1 (HIV-1) provirus in dendritic cells (DCs) occur through similar or common signaling pathways.
Methods: Phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 cells were used as the in vitro model of DCs. The activation of the DC-SIGN promoter and HIV-1 5' long-term repeat (LTR) sequence induced by interleukin 4 (IL-4) in differentiated THP-1 cells was studied using luciferase reporter plasmids. The regulatory signaling pathways were identified using specific inhibitors, and the activity of the DC-SIGN promoter and HIV-1 5'LTR was detected.
Results: HIV-1 5'TR was activated by IL-4 induced signaling pathways but much weaker than DC-SIGN promoter. 1L-4 induced activation of HIV-1 5'LTR was mainly through the nuclear factor kappa-light-chain-enhancer of activated B cells (NP-kappa B) pathway, which was also involved in activation of the DC-SIGN promoter. The extracellular signal-regulated kinase (ERK) pathway, which was the main pathway for DC-SIGN promoter activation, also played an important role in HIV-1 5'LTR activation.
Conclusion: Our study suggests that the activation of the DC-SIGN promoter and HIV-1 5'LTR may share NF-kappa B and ERK-signaling pathways.
