Research ArticleMALARIA

Activation of mosquito complement antiplasmodial response requires cellular immunity

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Science Immunology  20 Jan 2017:
Vol. 2, Issue 7, eaal1505
DOI: 10.1126/sciimmunol.aal1505

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More than a vector

Mosquitoes—the bane of lovers of the outdoors—are also carriers of serious diseases, including malaria, dengue, and Zika virus. Why does the mosquito itself not succumb to infection? Castillo et al. now report that the mosquito immune response to Plasmodium requires cellular immunity. They found that midgut nitration that results from Plasmodium infection in mosquitoes triggered the release of hemocyte-derived microvesicles and that these microvesicles were necessary for the activation of the mosquito complement-like system, which limits Plasmodium infection. Nitration-mediated hemocyte activation may parallel innate immune response to tissue damage in other organisms and shows a clear role for cellular immunity in the mosquito response to infection.


The mosquito complement-like system is a major defense mechanism that limits Plasmodium infection. Ookinete midgut invasion results in irreversible damage to invaded cells and triggers epithelial nitration and complement activation. Several lines of evidence suggest that hemocytes participate in early antiplasmodial responses that target ookinetes, but their role remains unclear. The fate of hemocytes in response to Plasmodium infection was investigated by labeling this cell population in vivo. We found that midgut nitration triggers the local release of hemocyte-derived microvesicles (HdMv) into the basal labyrinth of the midgut. Several different strategies, such as gene silencing, immune priming, or systemic injection of polystyrene beads, were used to either enhance or reduce HdMv release. We provide direct experimental evidence that contact of hemocytes with the nitrated midgut basal surface triggers HdMv release and that this response is necessary for effective activation of mosquito complement. Our studies suggest that hemocyte-derived microvesicles may deliver some critical factor(s) that promote activation of thioester-containing protein 1, a key effector of the mosquito antiplasmodial immunity.

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