Figure 7.

CCL-induced T_RM cells affect T cell responses by modifying the immune environment. Intestinal wormburden and fecal expulsion of helminth by WT mice and ccl25^−/− infected with N. brasiliensis are shown in panels (A) and (B), respectively. In panel (C), production of the indicated cytokine from in vitro worm antigen-stimulated mesenteric lymph node cultures. Expression of IFN-γ, IL-17, IL-10, IL-4, IL-13, and IL-33 mRNA in intestinal tissue from infected mice is shown in panel (D). n = 5 in each group. Data are representative of two independent experiments (mean ± SEM, ^*p < 0.05). Expression of MAdCAM-1 molecules by vascular endothelium in orthotopic PDAC is shown in panel (E). Mice were immunized with tumor cell lysates and syngeneic splenocyte with and without CCL25 a week before receiving intrapancreatic tumor cell implants. Panel F, weight of tumors excised 28 days after implantation. Tumor immune cell infiltrates were subsequently analyzed for the presence of CD3⁺ T cells (G) CD4⁺PD1⁺ T cells (H) and intensity of PF1 expression on these cells (I). The presence of Tgfβ mRNA was assessed by RT-PCR (J). In parallel experiment WT and CCL25-deficient mice were immunized with tumor cells and syngeneic splenocyte lysates a week before receiving intrapancreatic tumor cell implants. Panel (K), weight of tumors excised 28 days after implantation. Tumor immune cell infiltrates were subsequently analyzed for the presence of CD4⁺FoxP3⁺ cells (L), CD4⁺PD1⁺ cells (M) and intensity of PF1 expression on these cells (N) n > 5 N = 4 ^*p < 0.05; ^**p < 0.01.