Tumors derived factors significantly inhibit the generation as

well as the activation of dendritic cells (DCs). Polyinosinic-polycytidylic

acid (Poly I:C, PIC), a dsRNA analog, can trigger the secretion

of type I Interferon and induce apoptosis in tumor cells

via the innate recognition receptors melanoma-differentiationassociated

gene (MDA)-5 and retinod-inducible gene (RIG)-I

in the cytosol or via Toll-like receptors 3 in intracellular endosomes.

Thus, we hypothesized that prostate tumor cells activated

via these receptors could release soluble factors that can

restore the suppressive effect of tumor derived factors on DCs.

In order to see if factors secreted by PIC-stimulated DU145 cells

could somehow overcome this already described inhibitory effect,

DU145 cells were cultured with PIC-liposome complex (0.1

?Êg/ml) for 4 hours, washed three times with PBS, incubated for

20 additional hours and the culture supernatant was then harvested

and filtered (CM-PIC). As control, non stimulated DU145

cell culture supernatant was also collected (CM). Human monocyte-

derived DCs (MoDCs) cells were matured with LPS in the

presence of CM-PIC or CM. MoDCs stimulated with LPS in presence

of CM-PIC increased the expression costimulatory molecules

compared to MoDC stimulated with LPS in presence of CM

(CD86 MFI: 178 vs 97; CD80 MFI: 35 vs 26; CD40, MFI: 23 vs 14).

Furthermore, the levels of IL12p70 were significantly increased in

LPS-stimulated MoCDs incubated with CM-PIC at 24h (670.1�E}2.9

vs 90.3�E}16.3 pg/ml), and at 48h (926.5�E}14.2 vs 127.5�E}1.5 pg/ml),

p<0.05. MoDCs stimulated only with PIC (0.1 ?Êg/ml) did not

show any sign of maturation. Together, our results provide new

insights in the use of PIC-liposomes as therapeutic agents to

enhance the antitumoral immune response.