Fig. 1: Ferroptotic cell death, enhanced T cell infiltration and pro-inflammatory changes drive antitumour efficacy and synergize with ICB to inhibit B16-F10 tumour growth in particle-treated mice.

a–c, Ferroptosis study: B16-F10 tumour growth inhibition in mice following i.v. injection of αMSH-C′ dots (12 nmol per dose, Q3D×3 (60 μM), red), as against vehicle (blue) and αMSH-C′ dots + liproxstatin (liprox, green) on days 7, 10 and 14 post-implantation (a). Haematoxylin-and-eosin staining of tumour tissue specimens (scale bars, left panel, 1 mm; right panel, 100 μm) (b). Plots of pan T cell (CD3⁺), helper T cell (CD4⁺), cytotoxic (CD8⁺) T cell and macrophage (Iba1⁺) populations in the TME by IHC (c). d, Tumour growth inhibition in B16-F10 mice injected, as in a ± anti-PD-1 antibody (250 μg, n = 3 doses), using αMSH-C′ dots + anti-PD-1 (green), administered concomitantly, αMSH-C′ dots alone (red), anti-PD-1 alone (grey) or saline vehicle (blue). e, Plots of pan (CD3⁺), helper (CD4⁺) and cytotoxic (CD8⁺) T cell populations. f,g, Tumour growth in particle-treated B16-F10 tumour-bearing NOD-SCID (f) and NSG (g) mice using the regimen in a. Data reflect n = 4 mice per group for all animal studies, mean ± s.e.m. Non-parametric two-way ANOVA with Sidak’s post hoc test was performed for growth inhibition, and one-way ANOVA with Tukey’s test using multiple comparisons was performed for IHC quantification. All statistical tests were two-sided. *P < 0.05, **P < 0.01, ***P < 0.005 and ****P < 0.001.