Fig. 3: CCL3-mediated enhanced in vivo antitumor immunity caused by PGRN knockout.
From: Deciphering the potential role of PGRN in regulating CD8+ T cell antitumor immunity
A The treatment schedule for anti-CCL3 neutralizing antibody. B The measurements of tumor volume were conducted every two days, leading to the construction of growth curves (mean ± SEM; n = 5/group; *p < 0.05, ***p < 0.001). C In four different groups of mice, tumor weights were measured for subcutaneously transplanted tumors (n = 5/group, *p < 0.05, ****p < 0.0001). D The percentages of CD8+ T cells within the CD45+CD3+ cell population in tumor tissues were evaluated using the flow cytometry technique (n = 5/group; ****p < 0.0001). E Representative immunofluorescence staining with CD8 (red) and DAPI (blue) in tumor tissues from four mouse groups; scale bar = 50 μm. Flow cytometry was utilized to identify (F) IFN-γ, (G) GZMB, and (H) PD-1 expression in CD8+ T cells in all groups (n = 5/group; **p < 0.01, ****p < 0.0001 for IFN-γ and GZMB; *p < 0.05 for PD-1). I Using flow cytometry analysis, the percentage of apoptosis was determined among CD8+ T cells infiltrated in tumor tissue (n = 5/group; **p < 0.01; ****p < 0.0001).
