Our data implicate the activation of the adenosine A2B receptor during the infection by this parasite species to the inhibition of CD40 expression (14, 35), the lack of IL-12 production (16, 35), the phosphorylation of ERK1/2 (35, 36) (Figure 7) and also provide an explanation (increased cAMP) for the inhibition of the immune response by this parasite in the absence of a Th2 response (3) and IL-10 production (20, 60). The gene discussed is IL10; the disease is infection.