Ji-Yeon Park

Dong-A University, Pusan, Busan, South Korea

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Publications (3)7.25 Total impact

  • [show abstract] [hide abstract]
    ABSTRACT: Dendritic cells (DCs) are the most potent antigen-presenting cells (APCs) for naive T cells and play an important role in cancer immunology. All-trans retinoic acid (ATRA) is known to be a differentiating agent in the treatment of acute promyelocytic leukemia (APL). In this study, we investigated whether ATRA can differentiate the retinoic acid (RA)-sensitive promyelocytic leukemic cell line, NB4, to DC-like cells and whether these differentiated cells can activate T cells. NB4 cells were differentiated to myeloid cells by 4, 6, and 8 days of ATRA treatment. NB4 cells up-regulated markers found in DCs, including HLA-DR, costimulatory molecules (CD80 and CD86), adhesion molecules (CD40), and chemokine receptors (CCR6) when cultured for 8 days in the presence of 1 microM ATRA. Upregulation of CD83 was also detected on the surface of ATRA-treated NB4 cells versus untreated cells. The addition of cytokines alone, such as GM-CSF or CD40 ligand, did not affect the expression of CD83 in untreated NB4 cells but they up-regulated CD83 in ATRA-treated cells. CD11b was coexpressed with CD80, CD83, and CD86 in ATRA-treated NB4 cells. In a functional assay, ATRA-treated NB4 cells stimulated T cell proliferation when challenged with Staphylococcus enterotoxin B. These results suggest that the differentiation of NB4 cells by ATRA causes the cells to express DC markers, and that ATRA-differentiated NB4 cells are able to present antigens to T cells.
    International Immunopharmacology 01/2005; 4(13):1587-601. · 2.42 Impact Factor
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    ABSTRACT: Histamine receptors are expressed on neutrophils, and therefore, are likely to modulate neutrophil function. In this study, we investigated whether histamine modulates human neutrophil survival. Neutrophils were found to rapidly undergo spontaneous apoptosis upon culture in vitro and this was accelerated by high concentrations of histamine. Moreover, the percentage of apoptotic neutrophils was also markedly increased by treating with 10 mM histamine in the presence of inflammatory mediators, such as lipopolysaccharide (LPS), granulocyte macrophage-colony stimulating factor (GM-CSF), dibutyryl-cAMP (db-cAMP), or dexamethasone. Histamine-induced neutrophil apoptosis was inhibited by pyrilamine, a histamine receptor 1 antagonist, and by ranitidine, a selective histamine receptor 2 antagonist. In addition, diphenylene iodonium (DPI), an inhibitor of NADPH-oxidase, significantly blocked the apoptotic effect of histamine. Moreover, the induction of apoptosis by histamine was almost completely inhibited by zVAD-fmk, a pan-caspase inhibitor. In addition, immunoblotting showed that histamine induced the proteolytic activation of procaspase-3 in cell lysates treated with histamine. And, the protein kinase C (PKC)-delta inhibitor, rottlerin (5 microM) significantly blocked the apoptotic effect of histamine, though the cleavage of PKC-delta in 20 h cultured neutrophils was increased by histamine. However, an inhibitor of conventional PKC, Go6976 (100 nM) and a p38 mitogen-activated protein kinase inhibitor, SB203580 (10 microM), failed to block histamine-induced neutrophil apoptosis. These results suggest that high concentrations of histamine in local inflammatory and allergic lesions induce neutrophil apoptosis, and that this histamine-induced apoptosis is mediated by caspase activation and PKC-delta signaling.
    International Immunopharmacology 11/2003; 3(10-11):1491-502. · 2.42 Impact Factor
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    ABSTRACT: Neutrophil apoptosis is a constitutive process that can be enhanced or delayed by various stimuli. In this study, the effect of brefeldin A (BFA), which affects the biological process of secretion, on constitutive and delayed apoptosis of neutrophils was investigated. Neutrophil apoptosis was determined after culturing for 20 h in vitro by morphological changes, annexin V staining, and DNA electrophoresis. BFA dose-dependently increased the constitutive apoptotic rate of neutrophils. The delay of apoptosis induced by granulocyte-macrophage colony-stimulating factor (GM-CSF) and lipopolysaccharide (LPS) was also blocked by BFA. However, this effect of BFA was less marked when neutrophils were treated with dexamethasone, interleukin-8 (IL-8), or dibutyryl cAMP (dbcAMP). Moreover, the delay of neutrophil apoptosis induced by rottlerin, a specific inhibitor of protein kinase C (PKC)-delta, was significantly abrogated by BFA. Although BFA-induced apoptosis was not blocked by the caspase-3 inhibitor, zDEVD-fmk, myeloid cell leukemia-1 (Mcl-1) expression levels were downregulated by BFA. These results suggest that derangement of vesicular protein transport may be involved in the apoptosis of neutrophils, and that the action of BFA on apoptosis is dependent on changes in the expression of Mcl-1.
    International Immunopharmacology 07/2003; 3(6):835-43. · 2.42 Impact Factor

Publication Stats

18 Citations
126 Views
7.25 Total Impact Points

Institutions

  • 2003–2005
    • Dong-A University
      • College of Medicine
      Pusan, Busan, South Korea
    • National Cancer Center Korea
      Kōyō, Gyeonggi Province, South Korea