Figure 4

Poly(I:C) stimulates Type I IFNs that inhibit Chi3l1 expression and pulmonary melanoma metastasis and regulates the expression of upstream genes of Chi3l1.

WT, MAVS null (MAVS^−/−) or IFN-α/β receptor 1 null mice (IFNAR1^−/−) mice were given B16 melanoma cells or vehicle and treated with Poly(I:C) or vehicle. (a,b) The levels of IFN-α and IFN-β in BAL fluids from lungs from these mice were evaluated by ELISA. (c) BAL Chi3l1 protein was quantitated by ELISA in BAL fluids from lungs from WT (+/+) and IFNAR1 null mice (−/−) that had been given vehicle or melanoma cells and treated with Poly(I:C) or vehicle control. (d,e) Representative lungs and pleural melanoma counts in WT (+/+) and IFNAR1 null mice (−/−) that were given melanoma cells and treated with Poly(I:C) or vehicle control. (f–h) The levels of mRNA encoding Sema7a, β1 integrin (Itg-β1) and plexin C1 were evaluated by qRT-PCR in the WT mice 2 weeks after B16 melanoma cells or Poly(I:C) treatment. The values in the panels a–c and e–h represent the mean ± SEM of evaluations with a minimum of 4 mice. Panel d is representative of a minimum of 5 similar evaluations. **P < 0.01. ns, not significant.