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Enhancement of immunomodulatory activity by liposome-encapsulated natural phosphodiester bond CpG-DNA in a human B cell line

  • Kim, Dong-Bum (Department of Microbiology, College of Medicine, Hallym University) ;
  • Rhee, Jae-Won (Center for Medical Science Research, College of Medicine, Hallym University) ;
  • Kwon, Sang-Hoon (Department of Microbiology, College of Medicine, Hallym University) ;
  • Kim, Young-Eun (Department of Biochemistry, College of Natural Sciences, Chungbuk National University) ;
  • Choi, Soo-Young (Department of Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University) ;
  • Park, Jin-Seu (Department of Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University) ;
  • Lee, Young-Hee (Department of Biochemistry, College of Natural Sciences, Chungbuk National University) ;
  • Kwon, Hyung-Joo (Department of Microbiology, College of Medicine, Hallym University)
  • Published : 2010.04.30

Abstract

Natural phosphodiester bond CpG-DNA that contains immunomodulatory CpG motifs (PO-DNA) upregulates the expression of proinflammatory cytokines and induces an Ag-driven Th1 response in a CG sequence-dependent manner in mice. In humans, only phosphorothioate backbone-modified CpG-DNA (PS-DNA) and not PO-DNA has immunomodulatory activity. In this study, we found that liposome-encapsulated PO-DNA upregulated the expression of human $\beta$-defensin-2 (hBD-2) and major histocompatibility class II molecules (HLA-DRA) in a CG sequence-dependent and liposome- dependent manner in human B cells. Of the three different liposomes, DOTAP has the unique ability to enhance the immunomodulatory activity of PO-DNA. In contrast, HLA-DRA and hBD-2 promoter activation can be induced by liposome-encapsulated PS-DNA in a CG sequence-independent manner, depending on the CpG-DNA species. Our observations demonstrate that, when encapsulated with a proper liposome in the immune system, natural PO-DNA has the potential to be a useful therapy for the regulation of the innate immune response.

Keywords

References

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