Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells

Thumbnail Image
File version

Version of Record (VoR)

Akter, Jasmin
Khoury, David S
Aogo, Rosemary
Lansink, Lianne IM
SheelaNair, Arya
Thomas, Bryce S
Laohamonthonkul, Pawat
Pernold, Clara PS
Dixon, Matthew WA
Soon, Megan SF
Fogg, Lily G
Engel, Jessica A
Elliott, Trish
Sebina, Ismail
James, Kylie R
Cromer, Deborah
Davenport, Miles P
Haque, Ashraful
Griffith University Author(s)
Primary Supervisor
Other Supervisors
File type(s)

Plasmodium parasites invade and multiply inside red blood cells (RBC). Through a cycle of maturation, asexual replication, rupture and release of multiple infective merozoites, parasitised RBC (pRBC) can reach very high numbers in vivo, a process that correlates with disease severity in humans and experimental animals. Thus, controlling pRBC numbers can prevent or ameliorate malaria. In endemic regions, circulating parasite-specific antibodies associate with immunity to high parasitemia. Although in vitro assays reveal that protective antibodies could control pRBC via multiple mechanisms, in vivo assessment of antibody function remains challenging. Here, we employed two mouse models of antibody-mediated immunity to malaria, P. yoelii 17XNL and P. chabaudi chabaudi AS infection, to study infection-induced, parasite-specific antibody function in vivo. By tracking a single generation of pRBC, we tested the hypothesis that parasite-specific antibodies accelerate pRBC clearance. Though strongly protective against homologous re-challenge, parasite-specific IgG did not alter the rate of pRBC clearance, even in the presence of ongoing, systemic inflammation. Instead, antibodies prevented parasites progressing from one generation of RBC to the next. In vivo depletion studies using clodronate liposomes or cobra venom factor, suggested that optimal antibody function required splenic macrophages and dendritic cells, but not complement C3/C5-mediated killing. Finally, parasite-specific IgG bound poorly to the surface of pRBC, yet strongly to structures likely exposed by the rupture of mature schizonts. Thus, in our models of humoral immunity to malaria, infection-induced antibodies did not accelerate pRBC clearance, and instead co-operated with splenic phagocytes to block subsequent generations of pRBC.

Journal Title

PLoS Pathogens

Conference Title
Book Title




Thesis Type
Degree Program
Publisher link
Patent number
Grant identifier(s)
Rights Statement
Rights Statement

© 2019 Akter et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Item Access Status
Access the data
Related item(s)



Medical microbiology

Persistent link to this record

Akter, J; Khoury, DS; Aogo, R; Lansink, LIM; SheelaNair, A; Thomas, BS; Laohamonthonkul, P; Pernold, CPS; Dixon, MWA; Soon, MSF; Fogg, LG; Engel, JA; Elliott, T; Sebina, I; James, KR; Cromer, D; Davenport, MP; Haque, A, Plasmodium-specific antibodies block in vivo parasite growth without clearing infected red blood cells., PLoS Pathogens, 2019, 15 (2), pp. e1007599-