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Donate today to support women in science at Burnet and their work to unlock the vaginal microbiome and reduce risk of HIV infection and preterm birth for women around the world.
Infection with Plasmodium falciparum parasites causes the majority of malaria-related morbidity and mortality. Constant exposure to the pathogen leads to the acquisition of antibodies and high levels of antibodies have been associated with clinical protection against malaria. A possible protective mechanism is the opsonization of parasites, or malaria-infected erythrocytes (IEs), for phagocytic clearance. Current assays use adherent or chemically differentiated THP-1 cells to evaluate opsonic antibodies in patients' samples, but these assays are often time consuming and damage the effector cells. We have developed a high throughput flow cytometry-based phagocytosis assay using undifferentiated THP-1 cells to quantify the opsonic activity against late stage P. falciparum-IEs. Opsonic antibodies bound to IEs promote their phagocytic uptake through Fcgamma receptors found on THP-1 cells. Moreover, undifferentiated THP-1 cells do not express CD36, a surface scavenger receptor that promotes non-opsonic phagocytosis. This technical advance allows quantification of opsonic antibodies and is an important tool for the performance of large, population-based studies of malaria immunity, and to provide a significant increase in the statistical power for such studies.