Fig. 3: T cells from GPR171 KO mice are hyperactive to antigen stimulation.
From: The GPR171 pathway suppresses T cell activation and limits antitumor immunity
a GPR171 (β-gal) expression in thymus immune cells from naive WT or GPR171+/LacZ mice. b Flow cytometry analysis of GPR171 expression (β-gal) in activated CD4+ T cells from WT or GPR171+/LacZ mice. c Flow cytometry analysis of GPR171 expression (β-gal) in activated CD8+ T cells from WT or GPR171+/LacZ mice. d Flow cytometry analysis of GPR171 expression (β-gal) in splenic NK cells from WT or GPR171+/LacZ mice injected with poly I:C. e CFSE-labeled T cells from WT  or GPR171LacZ/LacZ mice were stimulated with titrated mCD3 mAb for 3 days. Cell division of CD4+ and CD8+T cells were quantified by CFSE dilution. f CFSE-labeled WT or GPR171LacZ/LacZ T cells were stimulated with mCD3 mAb and BigLEN for 3 days. Cell division of CD4+ and CD8+ T cells were quantified by CFSE dilution. g–i Splenocytes from WT or GPR171Lacz/LacZ mice were transferred into B6D2F1/J to induce GVH response. Donor T cells in peripheral blood were determined by flow cytometry (g). On day 10 after transfer, the numbers of graft T cells in the spleen were enumerated (h). The alloreactivity of splenocytes was evaluated by their 4-h killing capacity against CFSE-labeled BALB/c splenocytes (i). a n = 3 biologically independent samples. g, h and i n = 5 biologically independent sample. Statistical significance was determined by one-way ANOVA for a and two-tailed Student’s t-test for a, g, h, and i. Unless otherwise denoted, values are mean ± SEM. Source data was provided as a Source Data file. All data are representative of two independent experiments.
