At peak parasitemia, circulating pDCs were still functional in vitro, producing IFNα and TNF and upregulating CD86, HLA-DR, and CD123 following TLR7 and TLR9 stimulation [144], while CD1c+ cDCs expressed lower levels of HLA-DR, which correlated with less phagocytic capacity as well as impaired signaling following TLR or iRBC stimulation [143]. Here, TNF is linked to parasitic infectious disease.