Fig. 8: mGluR4-mediated glutamatergic signaling suppresses the function of human DCs.

A The RNA level of mGluR4 in human CD4⁺ T, CD8⁺ T cells, CD14⁺ monocytes, mo-DCs, and mo-Mac cells was analyzed by qPCR analysis (n = 5 healthy donors). B Human mo-DCs were treated with FM or HepG2 TCM for 24 h. The expression of GRM4 was determined (n = 3 biological replicates). C–E Human mo-DCs and (F–H) mo-Mac cells treated with ADX88178 (10 μM), UBP1112 (10 μM), or forskolin (10 μM) for 24 h were co-cultured with CTV-labeled human CD8⁺ T cells in the presence of anti-CD3 antibody (1 μg/ml) and IL-2 (100 U/ml) for 3 days. C The expression of CD80 and CD86 in mo-DCs (n = 6 biological replicates). D The total number of T cells (n = 3 biological replicates), and (E) the level of IFNγ in the cell culture supernatant (n = 4 biological replicates) after co-culture with mo-DCs. F The expression of CD80 and CD86 in mo-Mac cells (n = 4 biological replicates). (G) The total number of T cells (n = 3 biological replicates), and (H) the level of IFNγ in the cell culture supernatant (n = 4 biological replicates) after co-culture with mo-Mac cells. I The proliferation and number of CD8⁺ T cells treated with ADX88178 (10 μM), UBP1112 (10 μM), or forskolin (10 μM) (n = 3 biological replicates) in the presence of anti-CD3 antibody (1 μg/ml), anti-CD28 antibody (1 μg/ml) and IL-2 (200 U/ml) for 3 days, and (J) the level of IFNγ in the cell culture supernatant (n = 4 biological replicates). K Schematic of mGluR4-mediated glutamatergic signaling in DCs in modulating anti-tumor immunity. Data were presented as mean ± SEM. Statistical significance was determined by an unpaired t-test two-tailed (B–J). All biological experiments were repeated at least three times. Source data are provided as a Source Data file.