Protein Kinase C Blockade Inhibits Differentiation of Myeloid Blasts into Dendritic Cells by Calcium Ionophore A23187

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• 作者：Qian Li (1)
  Howard Ozer (1) (2)
  Inna Lindner (3)
  Kelvin P. Lee (3)
  Mohamed A. Kharfan-Dabajaa (2)
  
• 关键词：Protein kinase C ; Calcium ionophore A23187 ; Dendritic cells ; HL ; 60 myeloblasts
• 刊名：International Journal of Hematology
• 出版年：2005
• 出版时间：February 2005
• 年：2005
• 卷：81
• 期：2
• 页码：131-137
• 全文大小：409KB
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• 作者单位：Qian Li (1)
  Howard Ozer (1) (2)
  Inna Lindner (3)
  Kelvin P. Lee (3)
  Mohamed A. Kharfan-Dabajaa (2)
  
  1. Section of Hematology-Oncology, University of Oklahoma Health Sciences Center and OU Cancer Center, Oklahoma City
  2. Department of Medicine, University of Oklahoma Health Sciences Center, 920 Stanton L.Young Blvd, WP 2080, 73104, Oklahoma City, OK, USA
  3. Division of Hematology-Oncology and Department of Microbiology and Immunology, University of Miami, Miami, Florida, USA
  

文摘

Direct differentiation of myeloid leukemia blasts into antigen-presenting dendritic cells (DCs) for use as cellular vaccines is unique in that identification of tumor-specific antigens may not be necessary because the antigens should already be endogenously expressed.We hypothesized that signaling through protein kinase C (PKC) is required for differentiation of HL-60 promyeloblasts into DCs upon stimulation with calcium ionophore A23187. To demonstrate the inhibitory effect of PKC blockade, we pretreated HL-60 myeloid blasts with the protein kinase inhibitor bisindolylmaleimide I (Bis-1) for 24 hours and then treated the cells with calcium ionophore A23187 for an additional 24 hours. Controls consisted of HL-60 blasts treated with A23187, Bis-1 alone, or media.We noted that blasts cultured in media, Bis-1, or Bis-1 then A23187 did not develop the morphologic and phenotypic DC characteristics, up-regulate Rel B, or activate allogeneic T-cells. Our findings suggested that PKC blockade inhibits morphologic, phenotypic, and functional differentiation of HL-60 promyeloblasts into antigen-presenting DCs. Our findings supported the role of PKC as an obligatory pathway for calcium ionophore A23187-induced differentiation of HL-60 myeloblasts into antigen-presenting DCs.