iRBC- and TLR1/2 and TLR4 agonist-induced CD86 expression was also lower in CD1c+ cells isolated at peak parasitemia than prior to infection, while there was no change in TLR1/2 and TLR4-induced IL-12 expression and all three stimuli, iRBCs, TLR1/2 and TLR4 agonists, increased intracellular TNF [143]. Here, TNF is linked to parasitic infectious disease.