This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Barragan, A.
Right arrow Articles by Carlson, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barragan, A.
Right arrow Articles by Carlson, J.

 Previous Article  |  Next Article 

Infection and Immunity, May 2000, p. 2971-2975, Vol. 68, No. 5
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Blood Group A Antigen Is a Coreceptor in Plasmodium falciparum Rosetting

Antonio Barragan,1 Peter G. Kremsner,2,3 Mats Wahlgren,1,* and Johan Carlson1

Microbiology and Tumor Biology Center, Karolinska Institutet, and Swedish Institute for Infectious Disease Control, Stockholm, Sweden1; Department of Parasitology, Institute of Tropical Medicine, University of Tübingen, Tübingen, Germany2; and Research Unit, Albert Schweitzer Hospital, Lambaréné, Gabon3

Received 20 October 1999/Returned for modification 15 December 1999/Accepted 27 January 2000

The malaria parasite Plasmodium falciparum utilizes molecules present on the surface of uninfected red blood cells (RBC) for rosette formation, and a dependency on ABO antigens has been previously shown. In this study, the antirosetting effect of immune sera was related to the blood group of the infected human host. Sera from malaria-immune blood group A (or B) individuals were less prone to disrupt rosettes from clinical isolates of blood group A (or B) patients than to disrupt rosettes from isolates of blood group O patients. All fresh clinical isolates and laboratory strains exhibited distinct ABO blood group preferences, indicating that utilization of blood group antigens is a general feature of P. falciparum rosetting. Soluble A antigen strongly inhibited rosette formation when the parasite was cultivated in A RBC, while inhibition by glycosaminoglycans decreased. Furthermore, a soluble A antigen conjugate bound to the cell surface of parasitized RBC. Selective enzymatic digestion of blood group A antigen from the uninfected RBC surfaces totally abolished the preference of the parasite to form rosettes with these RBC, but rosettes could still form. Altogether, present data suggest an important role for A and B antigens as coreceptors in P. falciparum rosetting.


* Corresponding author. Mailing address: Microbiology and Tumor Biology Center, Box 280, Karolinska Institutet, S-171 77 Stockholm, Sweden. Phone: 46-8-4572510. Fax: 46-8-310525. E-mail: mats.wahlgren{at}smi.ki.se.


Infection and Immunity, May 2000, p. 2971-2975, Vol. 68, No. 5
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:

  • Fry, A. E., Griffiths, M. J., Auburn, S., Diakite, M., Forton, J. T., Green, A., Richardson, A., Wilson, J., Jallow, M., Sisay-Joof, F., Pinder, M., Peshu, N., Williams, T. N., Marsh, K., Molyneux, M. E., Taylor, T. E., Rockett, K. A., Kwiatkowski, D. P. (2008). Common variation in the ABO glycosyltransferase is associated with susceptibility to severe Plasmodium falciparum malaria. Hum Mol Genet 17: 567-576 [Abstract] [Full Text]  
  • Rowe, J. A., Handel, I. G., Thera, M. A., Deans, A.-M., Lyke, K. E., Kone, A., Diallo, D. A., Raza, A., Kai, O., Marsh, K., Plowe, C. V., Doumbo, O. K., Moulds, J. M. (2007). Blood group O protects against severe Plasmodium falciparum malaria through the mechanism of reduced rosetting. Proc. Natl. Acad. Sci. USA 104: 17471-17476 [Abstract] [Full Text]  
  • Cserti, C. M., Dzik, W. H. (2007). The ABO blood group system and Plasmodium falciparum malaria. Blood 110: 2250-2258 [Abstract] [Full Text]  
  • Ferreira, M. U., da Silva Nunes, M., Wunderlich, G. (2004). Antigenic Diversity and Immune Evasion by Malaria Parasites. CVI 11: 987-995 [Full Text]  
  • Struik, S. S., Omer, F. M., Artavanis-Tsakonas, K., Riley, E. M. (2004). Uninfected erythrocytes inhibit Plasmodium falciparum-induced cellular immune responses in whole-blood assays. Blood 103: 3084-3092 [Abstract] [Full Text]  
  • Vogt, A. M., Barragan, A., Chen, Q., Kironde, F., Spillmann, D., Wahlgren, M. (2003). Heparan sulfate on endothelial cells mediates the binding of Plasmodium falciparum-infected erythrocytes via the DBL1alpha domain of PfEMP1. Blood 101: 2405-2411 [Abstract] [Full Text]  
  • MOMBO, L.-E., NTOUMI, F., BISSEYE, C., OSSARI, S., LU, C. Y., NAGEL, R. L., KRISHNAMOORTHY, R. (2003). HUMAN GENETIC POLYMORPHISMS AND ASYMPTOMATIC PLASMODIUM FALCIPARUM MALARIA IN GABONESE SCHOOLCHILDREN. Am J Trop Med Hyg 68: 186-190 [Abstract] [Full Text]  
  • Heddini, A., Pettersson, F., Kai, O., Shafi, J., Obiero, J., Chen, Q., Barragan, A., Wahlgren, M., Marsh, K. (2001). Fresh Isolates from Children with Severe Plasmodium falciparum Malaria Bind to Multiple Receptors. Infect. Immun. 69: 5849-5856 [Abstract] [Full Text]