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. Author manuscript; available in PMC: 2022 Aug 25.
Published in final edited form as: Cell Rep. 2022 Aug 16;40(7):111201. doi: 10.1016/j.celrep.2022.111201

Figure 5. cDC1 accumulation requires innate lymphoid support.

Figure 5.

(A) RT-PCR for NK cell-activating cytokine transcripts expressed by ex vivo magnetically separated CD11c+ cells from LLC-EV and LLC-Vkine tumors.

(B) RT-PCR profile of NKp46+ NK1.1+ cells flow-sorted from LLC-EV and LLC-Vkine tumors. Data are presented as mean ± SEM, n = 3 for each group.

(C) Schematic of the NK cell depletion experiment.

(D) Summary of cDC subset frequency by flow cytometric analysis in LLC-EV versus LLC-Vkine tumors after treatment with NK cell-depleting antibody (anti-ASGM1) or vehicle (PBS).

(E) Csf2 (GM-CSF) RT-PCR of RNA extracted from NKp46+ NK1.1+ cells flow-sorted from LLC-EV and LLC-Vkine tumors growing in WT or Batf3−/− hosts.

(F) Stromal localization of NCR1+ (NKp46+) cells in human lung cancers (chromogen, DAB; counterstain, hematoxylin). 40× objective: scale bar, 60 μm.

(G) Annexin V/7-AAD apoptosis assay of MutuDC1940-EV or -Vkine dendritic cells exposed to graded staurosporine concentrations with or without murine GM-CSF.

Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. In vitro experiments were performed in technical triplicates. In vivo cohort sizes are shown in individual panels. All experiments were reproduced independently at least twice.