Antimalarial responses in Anopheles gambiae: from a complement-like protein to a complement-like pathway.
Malaria transmission between humans depends on the ability of Anopheles mosquitoes to support Plasmodium development. New perspectives in vector control are emerging from understanding the mosquito immune system, which plays critical roles in parasite recognition and killing. A number of factors controlling this process have been recently identified, and key among them is TEP1, a homolog of human complement factor C3 whose binding to the parasite surface targets it for subsequent killing. Here, we review our current knowledge of mosquito factors that respond to Plasmodium infection and elaborate on the activity and mode of action of the TEP1 complement-like pathway.
UPR9022, CNRS, 15 rue Descartes, F-67084 Strasbourg, France.
Stéphanie A
SA
Blandin
Eric
E
Marois
Elena A
EA
Levashina
D000818:Animals; D000852:Anopheles / Q000235:genetics / Q000276:immunology* / Q000821:virology; D000962:Antimalarials / Q000737:chemistry / Q000276:immunology*; D003165:Complement System Proteins / Q000737:chemistry / Q000276:immunology; D005260:Female; D006790:Host-Parasite Interactions; D006801:Humans; D019476:Insect Proteins / Q000737:chemistry / Q000276:immunology*; D007303:Insect Vectors / Q000235:genetics / Q000276:immunology* / Q000821:virology; D016778:Malaria, Falciparum / Q000276:immunology*; D008297:Male; D010963:Plasmodium falciparum / Q000276:immunology
D000962:Antimalarials; D019476:Insect Proteins; D003165:Complement System Proteins