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KMID : 0578320120330040335
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Molecules and Cells
2012 Volume.33 No. 4 p.335 ~ p.341
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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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Ju Sung-Mi
Goh Ah-Ra
Kwon Dong-Joo
Youn Gi-Soo
Kwon Hyung-Joo
Bae Yong-Soo
Choi Soo-Young
Park Jin-Seu
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Abstract
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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. Previ-ous 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-?B 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-?B/AP-1-dependent pathways in human B cells.
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KEYWORD
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AP-1, B cells, beta-defensins, HIV, MAPK, NF-?B, Tat
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