Killing Malaria Parasites: How Mosquito Blood Cells Shape anti-Plasmodium Immunity

Monday, November 10, 2014 - 9:00am
Event Type: 

Vector Entomology interview seminar: E164 Lagomarcino Hall

Ryan Smith, Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD

Abstract: Mosquitoes of the genus Anopheles serve as the obligate vectors of the malaria parasite Plasmodium. The mosquito innate immune response is a major determinant of parasite developmental success in its vector and in disease transmission. To date, a number of components of the mosquito innate immune response have been described that modulate Plasmodium development, yet our understanding of the mechanisms that limit Plasmodium development remains limited. Evidence suggests that parasite numbers are largely influenced by an “early-phase” that targets ookinetes as they reach the basal lamina of the mosquito midgut through the exposure to complement-like components of the hemolymph, and a “late-phase” response that limits oocyst survival. Previous reports have implicated the role of a LITAF-like transcription factor (LL3) in the Anopheles gambiae immune response. Following LL3-silencing, oocyst numbers are significantly increased and confirm that LL3 is involved in the “late-phase” response. Further experiments provide new insights into late-phase immunity demonstrating that LL3 and the STAT pathway play major roles in determining oocyst survival by regulating mosquito blood cell (hemocyte) function. Future experiments will address the mechanisms of hemocyte activation to address a critical gap in our knowledge of the mosquito immune response to Plasmodium and the mechanisms that limit oocyst survival in the mosquito host.