Figure 2.

CAF-released CXCL10, CXCL12 and TGF-β are not involved in CAF-mediated modulation of chemokine receptors, but PGE₂ partially modulates CXCR4. Levels of (A) CXCL10, CXCL9 and CXCL11; (B) CCL5, CCL3, and CCL8; and (C) CXCL12, and MIF in CAF-conditioned medium (n = 6). (D–G) Frequencies of (left) CXCR3 and (right) CXCR4 expression in CD4⁺ and CD8⁺ T cells after adding different concentrations of (D) CXCL10 (10 pg/mL, 50 pg/mL, 100 pg/mL, 1 ng/mL); (E) CXCL12 (10 pg/mL, 100 pg/mL, 500 pg/mL, 1 ng/mL); (F) rTGFβ (10 pg/mL, 100 pg/mL, 1 ng/mL, 10 ng/mL); and (G) rPGE₂ (1 ng/mL, 10 ng/mL, 30 ng/mL, 50 ng/mL) to the PBMCs. (H,I) Frequencies of (right) CXCR3, (left) CXCR4 on CD4⁺ and CD8⁺ T cells cultured with CAFs after addition of the corresponding isotype, vehicle or the following blocking: (H) 5 μg/mL of anti-TGFβ to block TGF-β and (I) 20 μM of indomethacin to block PGE₂. Data are related to those of the control cultures without CAFs. (D–I) Dots and lines show paired samples. (D–G) Friedman’s test and (H,I) a paired t test were used to detect statistically significant differences * p  <  0.05, ** p  <  0.01.