Stimulation of TLR-3 oriented macrophages to an M1 phenotype, as evidenced by (i) upregulation in the expression of costimulatory molecules; (ii) inhibition of co-inhibitory receptors; (iii) induction of IL-6, IL-12, TNF-α, iNOs; (iv) enhancement in antigen uptake; (v) improvement in the ability to prime T cells; (vi) blocking the polarization of macrophages toward M2a and M2c subtype; and (vii) significant increase in vivo of M1 macrophages and regression in tumor growth. The gene discussed is IL6; the disease is neoplasm.