Supplementary Table 1, Figures 1-5 from Myeloid-Derived Suppressor Cells as an Immune Parameter in Patients with Concurrent Sunitinib and Stereotactic Body Radiotherapy

Supplementary Table 1. Characteristics of the enrolled patients. Supplementary Figure 1. PBMCs were obtained from patients enrolled in the clinical trials at time points A (pre-sunitinib treatment), B (7 days post-sunitinib treatment), and C (6-30 days post-SBRT). Supplementary Figure 2. The number of pSTAT1+ in CD33+CD14+CD16+ (upper panels) and CD33+CD14+CD16- (lower panels) cells in PBMC from all patients and sunitinib-responders and non-responders based on Tbet+ CD4 T cell-criteria, was determined at the indicated time points. (*p < 0.05; ***p < 0.001) Supplementary Figure 3. The percentage and cell numbers of CD33+CD11b+ Supplementary Figure 4. The percentage of Tbet-expressing CD4 and CD8 T cells in PBMC from all patients, and patients who were separated into sunitinib-responders and non-responders was determined at the indicated time points based on the myeloid cell-based classification Supplementary Figure 5.(A) Mouse monocytic MDSC were left untreated (red) or treated with sunitinib (250 nM, blue) for 48 hrs. The apoptotic cells (Annexin V+) and phosphorylated STAT3 were assessed by flow cytometry. (B) Flow cytometric histogram of CD206+ in CD33+CD14+CD16- (blue) and CD33+CD14+CD16+ (red) populations (left panel). Mean fluorescent intensity of CD206+ was shown on the right panel. (C) Human CD33+CD14+CD16- and CD33+CD14+CD16+ populations were sorted from total PBMC. The mRNA expression of iNOS, MRC1, ARG1 and ARG2 were standardized as the fold changes using CD33+CD14+CD16- population as the base line. (C) The suppressive activity of sorted human CD33+CD14+CD16+ cells against the proliferation of autologous CD4+ T cells in the presence or absence of arginase inhibitor (Nor-NOHA, 100microM) was presented. (*p < 0.05; ***p < 0.001)