Journal
CELL HOST & MICROBE
Volume 5, Issue 3, Pages 273-284Publisher
CELL PRESS
DOI: 10.1016/j.chom.2009.01.005
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Funding
- Centre National de la Recherche Scientifique [UPR 9022]
- Institut National de la Recherche Medicale
- French Ministry of National Education and Research
- Schlumberger Foundation for Education and Research
- EMBO Young Investigator Program
- EC FP6th Networks of Excellence BioMalPar
- National Institutes of Health [2P01I44220-06A1]
- Howard Hughes Medical Institute
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Plasmodium development within Anopheles mosquitoes is a vulnerable step in the parasite transmission cycle, and targeting this step represents a promising strategy for malaria control. The thioester-containing complement-like protein TEP1 and two leucine-rich repeat (LRR) proteins, LRIM1 and APL1, have been identified as major mosquito factors that regulate parasite loads. Here, we show that LRIM1 and APL1 are required for binding of TEP1 to parasites. RNAi silencing of the LRR-encoding genes results in deposition of TEP1 on Anopheles tissues, thereby depleting TEP1 from circulation in the hemolymph and impeding its binding to Plasmodium. LRIM1 and APL1 not only stabilize circulating TEP1, they also stabilize each other prior to their interaction with TEP1. Our results indicate that three major antiparasitic factors in mosquitoes jointly function as a complement-like system in parasite killing, and they reveal a role for LRR proteins as complement control factors.
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