title: [Anti-tumor mechanisms of Sp2/0 tumor vaccine transfected with mIL-21 gene in mice].
abstract: OBJECTIVE
  To explore the anti-tumor mechanism of Sp2/0-mIL-21 tumor vaccine in mice.
  
  
  METHODS
  The molecules of MHC-I and CD80 on the surface of Sp2/0-mIL-21 tumor vaccine were detected by flow cytometry (FCM) respectively. A flow cytometric CFSE-7-AAD cytotoxicity assay was used to detect the cytotoxic activities of NK cells and CTLs. The expression of I-TAC in the tumor tissue was tested by RT-PCR.
  
  
  RESULTS
  The expression of MHC-I molecule on the surface of tumor vaccine was up-regulated obviously. The cytotoxic activities of NK cells and CTLs were significantly enhanced in the mice inoculated with Sp2/0-mIL-21 tumor vaccine compared with the mice inoculated with Sp2/0 tumor cell in control group. The expression of I-TAC in the tumor tissue was up-regulated. The histopathologic section analysis showed more lymphocytes were infiltrated in the tumor tissue.
  
  
  CONCLUSIONS
  Sp2/0-mIL-21 tumor vaccine can induce strong cell-mediated immune response to tumor cells after it was inoculated s.c into mice. The anti-tumor mechanisms induced by Sp2/0 tumor cell vaccine are associated with the proliferation and activation of T lymphocyte, the differentiation and maturity of NK cell, the infiltration of lymphocytes in tumor tissue, and the enharuement of cytotoxic activities of NK cells and CTLs.
authors.affiliation: Department of Pathogenic Biology and Immunology, Southeast University, Nanjing 210009, China.
authors.forename: Li-li
authors.initials: LL
authors.lastname: Chu
authors.forename: Jun
authors.initials: J
authors.lastname: Dou
authors.forename: Feng-shu
authors.initials: FS
authors.lastname: Zhao
authors.forename: Quan
authors.initials: Q
authors.lastname: Tang
authors.forename: Ai-feng
authors.initials: AF
authors.lastname: Zhang
authors.forename: Yong-fang
authors.initials: YF
authors.lastname: Wang
authors.forename: Ning
authors.initials: N
authors.lastname: Gu
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000276:immunology*; D018122:B7-1 Antigen / Q000276:immunology / Q000378:metabolism; D019496:Cancer Vaccines / Q000276:immunology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D054371:Chemokine CXCL11 / Q000235:genetics; D005260:Female; D005434:Flow Cytometry; D015395:Histocompatibility Antigens Class I / Q000276:immunology / Q000378:metabolism; D007111:Immunity, Cellular / Q000276:immunology; D007378:Interleukins / Q000235:genetics*; D007694:Killer Cells, Natural / Q000276:immunology / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011897:Random Allocation; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013154:Spleen / Q000166:cytology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology / Q000378:metabolism; D000098546:Interleukin-21
chemical_list: D000970:Antineoplastic Agents; D018122:B7-1 Antigen; D019496:Cancer Vaccines; D054371:Chemokine CXCL11; C515203:Cxcl11 protein, mouse; D015395:Histocompatibility Antigens Class I; D007378:Interleukins; D000098546:Interleukin-21