H2-Aa–deficient cDC2 are necessary for melanoma inhibition in H2-Aa ^cit/cit mice. Tumor growth curves of B16F10 melanoma after s.c. inoculation on day 0 into the flank of mice. No PD1 antibody was administered. (A and B) Lethally irradiated WT or H2-Aa^cit/cit(cit) recipients of WT (CD45.1), or H2-Aa^cit/cit (cit, CD45.2), or a 1:1 mixture of H2-Aa^cit/cit and WT bone marrow were inoculated with B16F10 cells 12 wk after bone marrow transfer (n = 7 or 8 recipients per group). (C–F) Mice in which H2-Aa was deleted in (C) DC (H2-Aa^flox/flox;Cd11c-cre), (D) B cells (H2-Aa^flox/flox;Cd19-cre), (E) macrophages (H2-Aa^flox/flox;LysM-cre), or (F) cDC1 (H2-Aa^flox/flox;Xcr1-cre). (C–F, n = 5–10 mice per group). H2-Aa^cit/cit;Xcr1-cre mice in F were checked by flow cytometric analysis to confirm the absence of undesired H2-Aa KO in B cells (pre-experiment) and cDC2 cells (post-experiment) to exclude any H2-Aa germline deletion due to Xcr1-cre leakage (Ferris et al., 2020; Lança et al., 2022; Wohn et al., 2020). Data are representative of two independent experiments (A–F). WT C57BL/6J mice from JAX (C–F) were used as controls. Error bars indicate SEM (A–F). P values were determined by two-way ANOVA with post-hoc Tukey test (A–F). *P < 0.05; **P < 0.01; ****P < 0.0001.