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  • Title: [Butyrophilin 3A1 (BTN3A1) enhances activation and proliferation of human peripheral blood Vγ9Vδ2 T cells induced by MTB-HAg].
    Author: Tang J, Sun J, Zha C, Chang J, Hu K, Fang Q, Chen Y, Chen J, Li B.
    Journal: Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi; 2020 Aug; 36(8):680-686. PubMed ID: 32958123.
    Abstract:
    Objective To investigate the role of butyrophilin 3A1 (BTN3A1) in the activation and proliferation of human peripheral blood Vγ9Vδ2 T cells induced by M. tuberculosis heat resistant antigen (MTB-HAg). Methods Human peripheral blood mononuclear cells (PBMCs) were treated with BTN3A1 blocking antibody for 3 hours and then stimulated with MTB-HAg or phosphoantigen (PAg). At 24 hours of stimulation, the cells were collected to detect the expression of CD69 in Vγ9Vδ2 T cells by flow cytometry. At 20 hours of stimulation, the cells were collected to detect the proportions of cells producing helper T cell type I (Th1) cytokines IFN-γ and tumor necrosis factor α (TNF-α) in the Vγ9Vδ2 T cells. The PBMCs were also stimulated and cultured in IL-2-containing medium for 10 days, and the expansion and proliferation activity of Vγ9Vδ2 T cells were detected. Results After stimulated with MTB-HAg, the average fluorescence intensity of CD69 and the proportion of CD69 positive cells in Vγ9Vδ2 T cells decreased significantly in BTN3A1 blocked group, being 13.84% and 43.00% of those in the stimulated group, respectively. However, the average fluorescence intensity of CD69 molecules and the proportion of positive cells in PAg blocked group were significantly inhibited (3.10%, 4.47% and 9.53%, 10.91% of those in the stimulated group). The proportions of IFN-γ and TNF-α producing Vγ9Vδ2 T cells stimulated with MTB-HAg decreased significantly in the BTN3A1 blocked group, and the expansion number and cell proliferation activity of Vγ9Vδ2 T cells were also reduced significantly in the BTN3A1 blocked group. The results were similar to those of the PAg blocked group. Conclusion BTN3A1 promotes activation and proliferation of peripheral blood Vγ9Vδ2 T cells induced by MTB-HAg.
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