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Blood, Vol. 95 No. 2 (January 15), 2000:
pp. 674-682
Multiple human serum components act as bridging molecules in
rosette formation by Plasmodium falciparum-infected
erythrocytes
Elizabeth A. Somner,
Julie Black, and
Geoffrey Pasvol
From the Department of Infection and Tropical Medicine, Imperial
College School of Medicine, Middlesex, United Kingdom.
Rosetting, the binding of parasitized erythrocytes to 2 or more
uninfected erythrocytes, is an in vitro correlate of disease severity
in Plasmodium falciparum malaria. Although cell ligands and
receptors have been identified and a role for immunoglobulin M has been
suggested, the molecular mechanisms of rosette formation are unknown.
The authors demonstrate unequivocally that rosette formation by P
falciparum-infected erythrocytes is specifically dependent on
human serum, and they propose that serum components act as
bridging molecules between the cell populations. Using heparin
treatment and Percoll density gradient centrifugation, they have
developed an assay in which parasitized erythrocytes grown in
serum-containing medium and optimally forming rosettes are stripped of
serum components. These infected cells were no longer able to form
rosettes when mixed with erythrocytes and incubated in serum-free
medium. Rosette formation was restored by the addition of serum or
certain serum fractions obtained by concanavalin A (conA) affinity,
anti-IgM affinity, anion exchange, and gel filtration chromatography.
The authors clearly demonstrate that multiple serum components IgM and
at least 2 othersare involved in rosette formation. Those others
consist of 1 or more acidic components of high-molecular mass that
binds to conA (but that is not thrombospondin, fibronectin, or von
Willebrand's factor) and of at least 1 more basic, smaller component
that does not bind to conA. Data on the size and number of
rosettes formed support the authors' hypothesis that multiple bridges
are involved in this complex cellular interaction. These findings have
important implications for the understanding of pathogenic adhesive
interactions of P falciparum and host susceptibility to severe malaria.
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