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Myeloid Cell Isolation from Mouse Skin and Draining Lymph Node Following Intradermal Immunization with Live Attenuated Plasmodium Sporozoites
Published on: May 18, 2016
Activation of mosquito complement antiplasmodial response requires cellular immunity
Julio César Castillo1, Ana Beatriz Barletta Ferreira1, Nathanie Trisnadi1
1Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20892, USA.
Mosquitoes release microvesicles from hemocytes upon Plasmodium infection, which are crucial for activating the mosquito complement system and fighting malaria parasites.
Area of Science:
- Immunology
- Entomology
- Parasitology
Background:
- The mosquito complement-like system is vital for limiting Plasmodium infection.
- Hemocytes are suspected to play a role in early anti-Plasmodium responses, but their exact function is unknown.
Purpose of the Study:
- To investigate the role and fate of hemocytes during Plasmodium infection in mosquitoes.
- To elucidate the mechanism by which hemocytes contribute to anti-Plasmodium immunity.
Main Methods:
- Hemocyte populations were labeled in vivo to track their response to Plasmodium infection.
- Hemocyte-derived microvesicle (HdMv) release was manipulated using gene silencing, immune priming, and polystyrene bead injection.
- The impact of HdMv release on complement activation was assessed.
Main Results:
- Midgut nitration, induced by ookinete invasion, triggers the release of HdMvs into the midgut basal labyrinth.
- HdMv release is directly linked to hemocyte contact with the nitrated midgut basal surface.
- This HdMv release is essential for the effective activation of the mosquito complement system.
Conclusions:
- Hemocyte-derived microvesicles are critical mediators of the mosquito's anti-Plasmodium immune response.
- HdMvs likely deliver factors that activate thioester-containing protein 1, a key component of mosquito antiplasmodial immunity.
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