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. Author manuscript; available in PMC: 2022 Feb 12.
Published in final edited form as: Nature. 2021 Nov 3;599(7886):673–678. doi: 10.1038/s41586-021-04057-2

Fig. 4 |. DDR1 as a therapeutic target for tumour immunotherapy.

Fig. 4 |

a, Growth of E0771 Ddr1-KO tumour cells with huDDR1 in C57BL/6 hosts treated intratumorally with isotype IgG (control (ctrl); n = 17 tumours) or with anti-DDR1 antibody clone 9 (no. 9; n = 18 tumours). b, MMTV-PyMT spontaneous mammary tumour growth (accumulative tumour volume per mouse, C57BL/6), treated intraperitoneally in a ‘post-tumour’ scheme with control (n = 7 mice) or anti-DDR1 clone 9 antibody (n = 8 mice). c, d, CD8+ (c) and CD4+ (d) TILs from E07771 huDDR1-expressing Ddr1-KO tumours in b, normalized by per-gram tumour (n = 4 tumours per group). e, Antibody-treated E0771 tumours analysed by SHG, To-pro-3 staining, and collagen fibre individualization. Block arrows indicate tumour margins. Scale bar, 50 μm. f, g, Fibre alignment (f) and fibre length (g) (margin ctrl, n = 6 tumours; margin no. 9, n = 5 tumours; core ctrl, n = 4 tumours; core no. 9, n = 4 tumours). h, CD3+ T cells in antibody-treated KO + huDDR1 E0771 tumours (ctrl, n = 10 tumours; no. 9, n = 9 tumours). i, DDR1-ECD (blue oval)-remodelled collagen fibres (red curvy lines) forming an immune-excluding barrier. The intracellular region of DDR1 (yellow ovals) triggers downstream signal transduction. Values represent mean ± s.e.m. P values as indicated; two-tailed Student’s t-test for all tests except for tumour volumes (two-way ANOVA).