Fig. 1

Frequencies, suppressive function and gating strategy of PMN-MDSCs. a Progressors (PR) showed significantly higher PMN-MDSC frequencies than controllers (CO) (p = 0.0013), but there was no difference in the frequencies between PR patients and patients with lung carcinoma (BRO) (p = 0.87). (b + c) Significantly decreased percentages of proliferating CD8 T cells after coincubation with PMN-MDSCs compared to coincubation with PBMCs depleted in all patients (p = 0.0001) (b) and in PR (p = 0.0039) (c). The PBMCs depleted was set as 100%, and PMN-MDSCs were calculated as percentages thereof. d Histograms of a proliferation assay with significant inhibition of CD8 T cell proliferation by PMN-MDSCs in a sample from a patient with a low level of PMN-MDSCs (0.23%). e Representative dot plots and gating of PMN-MDSCs. Gating here is demonstrated by a patient with a very high frequency of PMN-MDSCs (CD66⁺ CD15⁺ cells: 8.05%). The first gate (first panel) is placed on the monocyte fraction in FSC and SSC. The main MDSC fraction is found in the population above the monocyte fraction (oval gate, first panel). The second panel shows the CD11b⁺ and CD14⁻ populations (upper left gate). PMN-MDSCs are defined as CD11b⁺ CD14⁻ CD66b⁺ CD15⁺ and are shown in the upper right gate of the third panel. Gating was performed according to Vollbrecht et al. [8] and Rieber et al. [37, 38]. f Histograms of a proliferation assay with only minimal inhibition by PMN-MDSCs from the patient shown in (e). [PR: n = 10; CO: n = 5; HC: n = 5; BRO: n = 6]