FIGURE 5.

Tumor‐infiltrating and tumor‐conditioned neutrophils induce protumorigenic IL‐17A‐producing Th subset polarization through a B7‐H2‐dependent manner. (A) Representative analysis of CD15⁺ neutrophil (green) and CD4⁺ T cell (red) interactions in tumor tissues of GC patients by immunofluorescence. Scale bars: 20 microns. (B) The correlations between B7‐H2⁺ neutrophils and IL‐17A in human GC tumors were analyzed. Results are expressed as the number of B7‐H2⁺ neutrophils per million total cells and IL‐17A concentration or IL‐17A expression in tumor tissues. (C) CFSE‐labeled peripheral CD4⁺ T cells of GC patients were co‐cultured for 4 days with autologous neutrophils from non‐tumor or tumor tissues with or without anti‐B7‐H2 antibody. Representative data and statistical analysis of proliferated IL‐17A‐producing CD4⁺ T cells and IL‐17A production were shown (n = 3). (D) CFSE‐labeled peripheral CD4⁺ T cells of donors were co‐cultured for 4 days with autologous NTCS‐conditioned neutrophils or TTCS‐conditioned neutrophils with or without anti‐B7‐H2 antibody. Representative data and statistical analysis of proliferated IL‐17A‐producing CD4⁺ T cells and IL‐17A production were shown (n = 3). Each dot in panel (B) represents one patient. *P < 0.05; **P < 0.01; ^n.s. P > 0.05 for groups connected by horizontal lines