Fig. 3

Blockade of CCL2-CCR2 axis suppresses monocyte infiltration, TAMs accumulation and tumorigenesis in ESCC mouse model. a Gene knockout of CCL2 in mouse reduces tumor incidence and multiplicity (n = 10). b Deletion of CCL2 in mouse suppresses infiltration of CD11b⁺CCR2⁺ monocyte and CD11b⁺F4/80⁺ TAMs in forestomach tumors (n = 5). c Deletion of CCL2 in mouse inhibited production of TAMs-associated cytokines (CCL2, IL-10, IL-12b, and IL-13) (n = 5). d, e and f Gene knockout of CCR2 reduces tumor incidence (e) and tumor numbers (f) in mouse forestomach (n = 12). g Infiltration of CD11b⁺Ly6C^high inflammatory monocyte elevated in CCR2^+/+ wild type mice and CCR2^+/− heterozygous mice is blocked in CCR2^−/− animals (n = 6). h CCR2 knockout suppresses production of inflammatory cytokines in tumors (n = 6). Data is shown by mean ± standard deviation, * indicates P < 0.05, ** indicates P < 0.01, when compared to the CCR2^+/+ control