Fig. 1

NLGP restores the TC-MSC-mediated inhibition of T cell proliferation and effector functions. T cells (CD8⁺ and CD4⁺) and DCs were isolated from naïve C57BL/6 mouse spleen and bone marrow, respectively, as described in the “Materials and methods” section. DCs and T cells (DC:T = 1:10) were cultured in the presence of either normal or TC-MSCs (MSC:T = 1:5) for 72 h, with or without NLGP or NLGP alone as indicated. a Expression of Ki-67 was analyzed on CD8⁺ and CD4⁺ T cells after 72 h by flow cytometry. Bar diagrams depict the mean ± SD of aggregate data obtained in six independent experiments performed. *p < 0.05; b IFNγ expression on T cells was analyzed by flow cytometry. Bar diagrams depict the mean ± SD of aggregate data obtained in six independent experiments performed. **p < 0.001; c Measurement of T cell proliferation after 72 h by [³H] thymidine incorporation assay. Bar diagrams show the mean ± SD of aggregate data obtained in six independent replicative experiments. *p < 0.05versus DC-induced T cells in the presence of TC-MSCs. d Purified CD8⁺ cells were cultured in the presence of either normal or TC-MSC for 72 h with or without NLGP. Cytotoxicity of these differentially exposed CD8⁺ T cells towards B16 melanoma cells was measured by LDH release assay. Aggregate data obtained from six independent experiments performed.*p < 0.05 versus DC-induced CD8⁺T cells in the presence of TC-MSC. e The expression of Ki67 and intracellular IFNγ on CD8⁺ and CD4⁺ T cells is depicted in representative histogram respectively