TLR3 and acute myeloid leukemia: For example, incubation of primary AML cells with the TLR7/8 agonist R-848 led to increased expression of MHC molecules, proinflammatory cytokine production, and enhanced stimulation of allogeneic NK, NKT, and T cells (128), and loading of AML cells with the TLR3 agonist polyriboinosinic polyribocytidylic acid [poly(I:C)] led to increased MHC expression, apoptosis, and proinflammatory cytokine production, and enhanced the maturation and activation of dendritic cells after their uptake (125, 128, 129).