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Infection and Immunity, April 2007, p. 1771-1777, Vol. 75, No. 4
0019-9567/07/$08.00+0 doi:10.1128/IAI.01514-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Hans Peter Beck,2
Mats Wahlgren,3 and
Hans U. Lutz1*
ETH Zurich, Institute of Biochemistry, Schafmattstrasse 18, CH 8093 Zurich, Switzerland,1 Swiss Tropical Institute, Socinstrasse 57, CH 4002 Basel, Switzerland,2 Karolinska Institute, Microbiology and Tumor Center, Stockholm, Sweden3
Received 20 September 2006/ Returned for modification 24 October 2006/ Accepted 21 January 2007
Rosetting of Plasmodium falciparum-infected red blood cells (parasitized RBC [pRBC]) with uninfected RBC has been associated in many studies with malaria morbidity and is one form of cytoadherence observed with malarial parasites. Rosetting is serum dependent for many isolates of P. falciparum, including the strains FCR3S1.2 and Malayan Camp studied here. We identified the three naturally occurring components of sera which confer rosetting. Complement factor D alone induced 30 to 40% of de novo rosetting. Its effect was additive to that of 0.5 mg/ml albumin and to that of 15 ng/ml of naturally occurring antibodies to the anion transport protein, band 3. The three components together mediated rosetting as effectively as 10% serum. De novo rosetting experiments showed that naturally occurring anti-band 3 antibodies as well as factor D were effective only when added to pRBC. Factor D appeared to cleave a small fraction of a protein expressed on the surface of pRBC.
Published ahead of print on 29 January 2007.
Present address: Institute of Pharmaceutical Sciences, ETH Zurich, Zurich, Switzerland.
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