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Figure 1: Overview to protozoan and DC interactions. Protozoan parasites and their products interact with TLRs on DC leading to their activation and release of proinflammatory cytokines and up-regulation of costimulatory molecules promoting a Th1 responses and the control of the infection. However, in some cases (T. gondii infection), this response can be later impaired by the same parasites through mechanisms that involve enhancement of SOCS proteins expression and downregulation of IL-12 production. In addition, interactions of parasite molecules with Siglecs and CLRs may be responsible of maintaining DC in an immature state and refractory to TLR stimuli, diminishing their proinflammatory response likely by using ERK and PI3K-dependent pathways. These DC may lead to activation of Treg responses that presumably favour parasite survival.