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Blood, 15 April 2002, Vol. 99, No. 8, pp. 2677-2684
PLENARY PAPER
Plasmodium yoelii uses the murine Duffy antigen
receptor for chemokines as a receptor for normocyte invasion and an
alternative receptor for reticulocyte invasion
Christine J. Swardson-Olver,
Tracey C. Dawson,
Robert C. Burnett,
Stephen C. Peiper,
Nobuyo Maeda, and
Anne C. Avery
From the Department of Pathology, College of Veterinary
Medicine and Biomedical Sciences, Colorado State University, Fort
Collins; Pathology and Laboratory Medicine, University of North
Carolina-Chapel Hill; and the Henry Vogt Cancer Institute, University
of Louisville, KY.
Erythrocyte invasion by malaria parasites is a complex multistep
process involving parasite and erythrocyte receptors. It is a critical
stage in the parasite life cycle and, therefore, a logical step in
which to intervene to prevent or ameliorate disease. Rodent models of
malaria, commonly Plasmodium yoelii, are frequently used
for studies of malaria pathogenesis. Little is known, however, about
the invasion machinery of rodent malaria parasites. We have found
previously that mice congenic for a region of chromosome 1, containing
the Duffy antigen/receptor for chemokines (DARC), have different
susceptibility to P yoelii infection. Because P
vivax, a human parasite, and P knowlesi, a simian
parasite, use DARC to enter human erythrocytes, we sought to identify
the role of the murine DARC in P yoelii invasion. Using a
novel in vivo invasion assay and DARC knock-out mice, we found that
DARC knock-out normocytes (mature erythrocytes) had negligible levels of P yoelii invasion compared with wild-type normocytes,
demonstrating that DARC is a receptor for invasion of murine
erythrocytes. In contrast, DARC knock-out reticulocytes were invaded at
a rate similar to that for wild-type reticulocytes. We conclude that there is a DARC- independent pathway for reticulocyte invasion. These
findings represent the first identification of a murine malaria
receptor on erythrocytes and the first determination that different
pathways of invasion exist on normocytes and reticulocytes. Because we
show conservation of host-receptor interactions between rodent and
human malaria, we can now use this model to identify how immunity can
interfere with the invasion process.
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