Extracellular HIV-1 Tat induces human beta-defensin-2 production via NF-kappaB/AP-1 dependent pathways in human B cells |
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Authors: | Sung Mi Ju Ah Ra Goh Dong-Joo Kwon Gi Soo Youn Hyung-Joo Kwon Yong Soo Bae Soo Young Choi Jinseu Park |
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Institution: | Department of Biomedical Science, Research Institute for Bioscience and Biotechnology, Hallym University, Chunchon 200-702, Korea. |
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Abstract: | Defensins, a family of antimicrobial peptides, are one of the first lines of host defense. Human beta-defensins (hBD) such
as hBD-2 and -3 have anti-HIV activity. Previous studies have shown that HIV-1 virion can induce the expression of hBD, although
the exact components of HIV-1 virion that are responsible for hBD expression have not yet been elucidated. In this study,
we examined the effect of HIV-1 Tat on the expression of hBD in B cells. Stimulation of B cells with HIV-1 Tat protein significantly
increased the mRNA and protein levels of hBD-2. HIV-1 Tat also induced the activation of a reporter gene for hBD-2 in a dose-dependent
manner in B cells. Pretreatment of B cells with a JNK inhibitor suppressed HIV-1 Tat-induced hBD-2 expression. Pretreatment
of B cells with AP-1 inhibitors or NF-κB inhibitors led to a decrease in HIV-1 Tat-induced protein and mRNA expression of
hBD-2. Taken together, our results indicate that HIV-1 Tat can up-regulate the expression of hBD-2 via JNK-NF-κB/AP-1-dependent pathways in human B cells. |
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Keywords: | LRR LRRTM slitrk synaptic cell adhesion |
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