Fig. 3. Tumour-infiltrated IL-17A-producing cells were mainly Vγ1 γδ T cells.
a, b Infiltrated cells from subcutaneous tumour of CT26 and A20 were isolated, followed by flow cytometry analysis as indicated (n = 17, P < 0.0001). c, d Infiltrated cells from tumour of CT26 (c), A20 (d) were isolated, followed by flow cytometry analysis as indicated (n = 16 for c and n = 16 for d). e Vγ1 γδ T cells were depleted by neutralizing antibody described in the Methods (80 μg/mouse), and CT26 tumour growth kinetics was shown (n = 13 for each group, P = 0.0351 for control vs control+α-Vγ1, P < 0.0001 for control vs α-BTNL2, NS for control+α-Vγ1 vs α-BTNL2 + α-Vγ1). The depletion effect of Vγ1 γδ T cells in the IEL was shown in the right panel (n = 7, P < 0.0001). f CT26 tumours were processed as in e, and IL-17A secretion by TME-infiltrated cells was measured by ELISA (n = 12, P < 0.0001 for control vs α-BTNL2, control+α-Vγ1 and α-BTNL2 + α-Vγ1). All data are mean ± s.e.m. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 based on two-sided Mann–Whitney test for (a, b), Two-way ANOVA for (e) and one-way ANOVA for (f). Data are representative of three independent experiments.