Fig. 5

CD11b⁺CD16⁺myeloid cells became immature neutrophils after therapy in capecitabine-resistant patients. a Peripheral venous blood from capecitabine-resistant and capecitabine-sensitive CRC patients was collected after the treatment in 6–9 months. CD11b⁺CD16⁺myeloid cells in sensitive patients and that of CD11b⁺CD16⁻ in resistant patients were sorted for further analysis in (b), (c) and (d). b Expression of myeloid-associated and hematopoietic progenitor-associated markers on CD11b⁺CD16⁺myeloid cells in sensitive patients and on CD11b⁺CD16⁻myeloid cells in resistant patients was analyzed by flow cytometry. c Peripheral blood CD11b⁺CD16⁺myeloid cells in sensitive patients and CD11b⁺CD16⁻myeloid cells in resistant patients were sorted and analyzed by RNA sequencing. Expression of neutrophil-related and monocyte-related genes derived from the results of RNA sequencing was shown in the heatmap. d GO enrichment terms of differentially expressed MDSC-related immunosuppressive biological processes derived from RNA sequencing. e Autologous T cells were cultured alone, cocultured with peripheral blood CD11b⁺CD16⁺myeloid cells (from HDs and sensitive CRC patients) or CD11b⁺CD16⁻myeloid cells (from resistant CRC patients) for 48 h, respectively. Proliferation of T cells were analyzed by flow cytometry after incubation (n = 3 for each group). CD16⁺N HD = CD11b⁺CD16⁺myeloid cells from HDs, CD16⁺N CRC S = CD11b⁺CD16⁺myeloid cells from sensitive CRC patients, CD16⁻N CRC R = CD11b⁺CD16⁻myeloid cells from resistant CRC patients. Mean ± SEM, *P<0.05, **P<0.01 by t tests (e)