Vector Protector

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Science  27 Oct 2006:
Vol. 314, Issue 5799, pp. 566-567
DOI: 10.1126/science.314.5799.566d

As with other vector-borne parasitic diseases, there are two sites at which an immune response might disrupt the lifestyle of the protozoan parasite Plasmodium falciparum: in the final host or in its arthropod vector. Indeed, the mosquito is fully capable of generating a robust antiparasitic response against the motile Plasmodium ookinete, which invades the insect's midgut to establish itself as an oocyst.

Frolet et al. reveal two pathways that contribute to the regulation of this response, presenting evidence that antiparasitic immunity is divided between two phases of parasite invasion. The pre-invasion stage is characterized by basal expression of two effectors: the complement-like thioester-containing protein 1 (TEP1) and leucine-rich repeat immune protein 1 (LRIM1), which increases in the ookinete invasion stage. The expression of both effectors could be inhibited by silencing the nuclear factor κB (NF-κB) family proteins Rel1 and Rel2, leading to an increase in parasite growth. Conversely, mosquito resistance increased upon inhibition of the IκB-related negative regulator Cactus, leading to high levels of parasite killing. This potent antiparasitic response within the mosquito vector—regulated by the balance between the negative effects of IκB/Cactus and the activation of two NF-κB/Rel transcription factors—could represent a target in the battle against malaria. — SJS

Immunity 25, 10.1016/j.immuni.2006.08.019 (2006).

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