Figure 2.

Proposed T. gondii sensing mechanism(s) utilized by human monocytes. Although T. gondii tachyzoites can infect host cells either actively by invasion or passively by being phagocytized, only the latter process results in proinflammatory cytokine secretion by human myeloid cells. Once the live parasite has been engulfed (1), endosomal acidification and recruitment of lysosomes to the phagosomes leads to the degradation of the parasite (2). Released parasite molecules may be recognized either by PRR-contacting endosomes trafficking to the phagolysosome (3a) or by PRR in the cytosol detecting parasite components leaked from the phagosome (3b). In the scenario/model indicated in 3a, T. gondii DNA and RNA interaction with endosomal TLR will activate the canonical NF-κB signaling pathway and trigger TNFα and IL-12 production. In the scenario/model shown in 3b, as a consequence of phagolysosome leakage, parasite RNA is recognized by cytosolic RLR, such as RIG-I or MDA-5, which signals through the MAVS-dependent pathway to promote secretion of these cytokines.