scholarly journals Both wild-type and strongly attenuated bovine leukemia viruses protect peripheral blood mononuclear cells from apoptosis.

1997 ◽  
Vol 71 (1) ◽  
pp. 630-639 ◽  
Author(s):  
F Dequiedt ◽  
E Hanon ◽  
P Kerkhofs ◽  
P P Pastoret ◽  
D Portetelle ◽  
...  

Author(s):  
Ian F. Parney ◽  
Maxine A. Farr-Jones ◽  
Kevin Kane ◽  
Lung-Ji Chang ◽  
Kenneth C. Petruk

Background:Cancer immunogene therapy is based on vaccination with radiated, autologous tumor cells transduced with immunostimulatory genes. To help determine an optimal glioma immunogene therapy strategy, we stimulated lymphocytes with autologous human glioma cells transduced with B7-2 (CD86), granulocyte-macrophage colony-stimulating factor (GM-CSF), and/or interleukin-12 (IL12).Methods:A human glioma-derived cell culture (Ed147.BT) was transduced with B7-2, GM-CSF, and/or IL12 using retroviral vectors. Autologous peripheral blood mononuclear cells (PBMC) were co-cultured with irradiated gene-transduced tumor alone or a combination of radiated wild type and gene-transduced cells. Peripheral blood mononuclear cells proliferation was determined by serial cell counts. Peripheral blood mononuclear cells phenotype was assessed by flow cytometry for CD4, CD8, and CD16. Anti-tumor cytotoxicity was determined by chromium-51 (51Cr) release assay.Results:Peripheral blood mononuclear cells cell numbers all decreased during primary stimulation but tumor cells expressing B7-2 or GM-CSF consistently caused secondary proliferation. Tumors expressing B7-2 and GM-CSF or B7-2, GM-CSF, and IL12 consistently increased PBMC CD8+ (cytotoxic T) and CD16+ (natural killer) percentages. Interestingly, anti-tumor cytotoxicity only exceeded that of PBMC stimulated with wild type tumor alone when peripheral blood mononuclear cells were stimulated with both wild type tumor and B7-2/GM-CSF- (but not IL12) transduced cells.Conclusion:PBMC proliferation and phenotype is altered as expected by exposure to immunostimulatory gene-transduced tumor. However, transduced tumor cells alone do not stimulate greater anti-tumor cytotoxicity than wild type tumor. Only B7-2/GM-CSF-transduced cells combined with wild type produced increased cytotoxicity. This may reflect selection of tumor subclones with limited antigenic spectra during retrovirus-mediated gene transfer.



2019 ◽  
Vol 11 (2) ◽  
pp. 200-4
Author(s):  
Meira Erawati ◽  
Nyoman Suci Widyastiti ◽  
Tri Indah Winarni ◽  
Edi Dharmana

BACKGROUND: In tuberculosis infections, the immune system is weakened and cannot produce enough cytokines to against the infection. b-glucan is a potent immunomodulator that induces cytokine production in various bacterial infections. This study aimed to determine the effects of b-glucan on the production of interferon (IFN)-γ and interleukin (IL)-12 in peripheral blood mononuclear cells (PBMCs) induced by Mycobacterium tuberculosis DNA.METHODS: PBMCs were isolated from 11 healthy subjects. PBMCs were treated with/without 5 μg/mL b-glucan and M. tuberculosis rpoB wild-type or mutant DNA. The production of IFN-γ and IL-12 in the supernatant was performed with enzyme-linked immune-sorbent assay (ELISA).RESULTS: b-glucan increased significantly (p<0.05) IFN-γ of M. tuberculosis mutant DNA-induced PBMCs, M. tuberculosis wild-type DNA-induced PBMCs, and non-induced PBMCs. b-glucan also increased significantly (p<0.05) IL-12 of M. tuberculosis mutant DNA-induced PBMCs, M. tuberculosis wild-type DNA-induced PBMCs, and non-induced PBMCs. There were not any significant difference between male and female groups for IL-12 and IFN-γ in all treatment groups (p>0.05, ANOVA test).CONCLUSION: This in vitro study indicates that b-glucan increases the performance of PBMCs to produce IFN-γ and IL-12, with/without induction of M. tuberculosis wild-type/ mutant DNA.KEYWORDS: b-glucan, IFN-γ, IL-12, M. tuberculosis, rpoB



Sign in / Sign up

Export Citation Format

Share Document