Fig. 3: rHGF (400 ng/mL) enhances DISC formation to promote Fas-mediated apoptosis in both naive and PHA-stimulated msCD8⁺ T cells.

A(a, b) c-Met expression in n-msCD8⁺ T cells at the protein (a, n = 3) and mRNA (b, n = 3) levels identified by FCM and qRT‒PCR assays, respectively. B(a–e) Immunofluorescence staining for Fas expression (red) in MACS-purified pn-msCD8⁺ T cells (denoted in blue) after 48 (a, b, boxes, arrows denote Fas aggregation) and 72 h (c, d, boxes) of 400 ng/mL rHGF treatment and quantification (e) compared with the PHA-control groups. Scale bar = 200 µM, n = 6/time point; C(a–d) IP with a Fas antibody followed by IB for FADD (a, n = 2), caspase-8 (b, n = 2), and caspase-3 (c, n = 2) of cell lysates only for Fas control protein (d, n = 2) after 48 h of 400 ng/mL treatment. D(a, b) MTT assay (a) and RT-qPCR (b) were used for the assessment of caspase-8 expression in the presence or absence of 400 ng/mL rHGF for 48 (b) and 72 h (a, b), n = 10. E(a, b) MTT assay (a) and RTq-PCR (b) were performed for the assessment of caspase-3 expression in the presence or absence of 400 ng/mL rHGF for 48 (b) and 72 h (a, b), n = 10. F Anti-CH11-mAb (250 ng/mL, red box) was selected for the treatment of Jurkat T cells (J) based on the experimental results to determine the ideal concentration, n = 2. At least three independent experiments were performed, and the data are presented as the means ± SDs; *p < 0.05 and **p < 0.001 vs. PHA-Ctrls; ns represents no significance (Student’s t test).