title: [Silencing of SOCS1 and IL-12 gene cotransferred by adenoviral enhances DC-mediated anti-laryngocarcinoma immunity in vitro].
abstract: OBJECTIVE
  To investigate the effects and the related immunological mechanisms of dendritic cells (DCs) modified by SOCS1siRNA gene and IL-12 gene on activating and inducing cytotoxic T lymphocyte (CTL) as well as specific immune critically killing laryngocarcinoma in vitro.
  
  
  METHODS
  DCs were derived from human peripheral blood mononuclear cells (hPBMC), modified by recombinant SOCSlsiRNA adenoviral and IL-12 adenoviral and then pulsed with tumor antigen of repeated freeze-thaw method. The IL-12 and IFN-y levels in culture supernatant of DCs and CTILs were examined by ELISA.
  
  
  RESULTS
  DC were cultivated successfully and had special morphologic haracteristicistics. The rate of Ad-GFP carrying fluorescent expression was over 90%. The expression of SOCS1 protein in DCs were effectively decreased by being modified SOCSlsiRNA and IL-12 genetic while the expression of IL-12 protein were increased. The secretion rate of IL-12 factor was higher than that of SOCSlsiRNA and IL-12 transfection of single gene respectively in modified DCs which could prompt T cell proliferation activation significantly as well. IFN-y was secreted constantly in DC and CTL, resulting in Hep-2.
  
  
  CONCLUSIONS
  DC modified by SOCSlsiRNA and IL-12 gene which pulsed with laryngeal carcinoma antigen could increased the production of IL-12 and IFN-y; DC modified by SOCSlsiRNA and IL-12 gene which pulsed with laryngeal carcinoma antigen could enhance the ability to stimulate proliferation of T cell, increase production of IFN-y, IL-12 by T cells and induce the stronger killing rate of CTL.
authors.affiliation: Liaoning Medical University, and Department of Otolaryngology, the First Affiliated Hospital of Liaoning Medical University, Jinzhou, China.
authors.forename: Yunxia
authors.initials: Y
authors.lastname: Li
authors.forename: Yang
authors.initials: Y
authors.lastname: Yuan
authors.forename: Xuefeng
authors.initials: X
authors.lastname: Wang
mesh_terms: D000256:Adenoviridae / Q000235:genetics; D000951:Antigens, Neoplasm / Q000276:immunology* / Q000378:metabolism; D002460:Cell Line; D003602:Cytotoxicity, Immunologic; D003713:Dendritic Cells / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D020868:Gene Silencing; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D018664:Interleukin-12 / Q000235:genetics* / Q000378:metabolism; D007822:Laryngeal Neoplasms / Q000276:immunology*; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000276:immunology; D008213:Lymphocyte Activation; D034741:RNA, Small Interfering; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics* / Q000378:metabolism; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D014162:Transfection
chemical_list: D000951:Antigens, Neoplasm; D034741:RNA, Small Interfering; C108944:SOCS1 protein, human; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D018664:Interleukin-12; D007371:Interferon-gamma