Immune response of dendritic cells acquiring antigens from apoptotic cholangiocarcinoma cells induced by mitomycin.
- Author:
Gang WU
1
;
Ben-li HAN
;
Xue-tao PEI
Author Information
- Publication Type:Journal Article
- MeSH: Antigens, Neoplasm; immunology; Apoptosis; drug effects; Bile Duct Neoplasms; immunology; pathology; Bile Ducts, Intrahepatic; Cholangiocarcinoma; immunology; pathology; Coculture Techniques; Dendritic Cells; drug effects; immunology; Granulocyte-Macrophage Colony-Stimulating Factor; pharmacology; Humans; Interleukin-4; pharmacology; Mitomycin; pharmacology; T-Lymphocytes; immunology; Tumor Cells, Cultured
- From: Chinese Journal of Hepatology 2003;11(3):149-152
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the anti-tumor immune response of dendritic cells (DCs) acquiring antigens from apoptotic cholangiocarcinoma cells and their therapeutic effects on cholangiocarcinoma cells.
METHODSDCs from human peripheral blood monocytes which acquired antigen capturing and processing capacity, characteristics of maturation, were established in vitro using granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4). Then cholangiocarcinoma cells were induced to apoptosis with mitomycin. The three groups included (1) coculture of DCs, apoptotic cancer cells and T cells, (2) coculture of DCs, necrotic cancer cells and T cells, (3) coculture of DCs, cultured cancer cells and T cells. After 7 days, DCs and T cells were riched separately to perform anti-tumor cells test and immune response test.
RESULTSthese cells had typical dendritic cell morphology, expressed high levels of CD1a and B7, acquired antigen from apoptotic cells caused by mitomycin and could stimulate T cells to inhibit, even kill cholangiocarcinoma cells.
CONCLUSIONSThe DCs from peripheral blood monocytes induced by GM-CSF and IL-4 can efficiently present antigen derived from apoptotic cells caused by mitomycin, and stimulate T cells activity obviously. It maybe become an effective therapy for tumor.