Molecules and Cells

, Volume 33, Issue 4, pp 335–341

Extracellular HIV-1 Tat induces human beta-defensin-2 production via NF-kappaB/AP-1 dependent pathways in human B cells

Authors

  • Sung Mi Ju
    • Department of Biomedical Science, Research Institute for Bioscience and BiotechnologyHallym University
  • Ah Ra Goh
    • Department of Biomedical Science, Research Institute for Bioscience and BiotechnologyHallym University
  • Dong-Joo Kwon
    • Department of Biomedical Science, Research Institute for Bioscience and BiotechnologyHallym University
  • Gi Soo Youn
    • Department of Biomedical Science, Research Institute for Bioscience and BiotechnologyHallym University
  • Hyung-Joo Kwon
    • Department of Microbiology, College of MedicineHallym University
  • Yong Soo Bae
    • Department of Biological Science, College of Natural SciencesSungkyunkwan University
  • Soo Young Choi
    • Department of Biomedical Science, Research Institute for Bioscience and BiotechnologyHallym University
    • Department of Biomedical Science, Research Institute for Bioscience and BiotechnologyHallym University
Article

DOI: 10.1007/s10059-012-2287-0

Cite this article as:
Ju, S.M., Goh, A.R., Kwon, D. et al. Mol Cells (2012) 33: 335. doi:10.1007/s10059-012-2287-0

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.

Keywords

AP-1 B cells beta-defensins HIV MAPK NF-κB Tat

Copyright information

© The Korean Society for Molecular and Cellular Biology and Springer Netherlands 2012