[Primary study on preparation and efficiency of neotype hepatocellular carcinoma-dendritic cell vaccine with SOCS1 expression inhibited].
OBJECTIVE
To investigate the effect of SOCS1 expression inhibition on hepatocellular carcinoma-dendritic cell vaccine stimulated by LIGHT.


METHODS
The dendritic cells (DC) were generated from mouse bone marrow (BMDC) by cultured in medium containing rmGM-CSF and rmIL-4. The vaccine cells were prepared by loaded with hepatocellular carcinoma HepA antigen and further treated with or without LIGHT and SOCS1 antisense oligonucleotide (AS1). For detecting the maturity of the vaccine cells, the expression of the cell's surface molecules CD40 and CD86 were measured by FACS, and IL-12 and IL-1 secretion from the cells were determined by ELISA. And the CTL activity, cellular proliferation, IL-6 and TNF-beta secretion levels of the vaccine-stimulated lymphocytes were also assessed for analyzing the immune response of lymphocyte.


RESULTS
CD40 and CD86 expression of the prepared vaccine cells were obviously enhanced by treatment of LIGHT and AS1, and so were IL-12 and IL-1 (P<0.01). It was also observed that CTL activity, cellular proliferation and IL-6 and TNF-beta secreting levels of lymphocytes that were stimulated by the vaccine cells treated with AS1 were notably enhanced.


CONCLUSIONS
Inhibiting SOCS1 can improve the maturation of hepatocellular carcinoma-DC vaccine cell and can increase its inducing ability of anti-cancer immune response.
Liu
Zhan-Pei
ZP
Department of General Surgery, West China Hospital, Sichuan University, Chengdu 610041, China.
Zhang
Jie
J
Lin
Ping
P
Wang
Xiu-Jie
XJ
Wang
Qi
Q
D000818:Animals; D051940:B7-2 Antigen / Q000378:metabolism; D019013:CD40 Antigens / Q000378:metabolism; D019496:Cancer Vaccines / Q000096:biosynthesis / Q000276:immunology*; D006528:Carcinoma, Hepatocellular / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D002478:Cells, Cultured; D003602:Cytotoxicity, Immunologic / Q000276:immunology; D003713:Dendritic Cells / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D007114:Immunization; D007375:Interleukin-1 / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008113:Liver Neoplasms / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008214:Lymphocytes / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D008233:Lymphotoxin-alpha / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D016376:Oligonucleotides, Antisense / Q000494:pharmacology; D011994:Recombinant Proteins / Q000494:pharmacology; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000096:biosynthesis* / Q000235:genetics; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14 / Q000235:genetics / Q000494:pharmacology
D051940:B7-2 Antigen; D019013:CD40 Antigens; D019496:Cancer Vaccines; D007375:Interleukin-1; D015850:Interleukin-6; D008233:Lymphotoxin-alpha; D016376:Oligonucleotides, Antisense; D011994:Recombinant Proteins; C491590:Socs1 protein, mouse; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins; C505915:Tnfsf14 protein, mouse; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14; D018664:Interleukin-12