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Infection and Immunity, September 2004, p. 5412-5418, Vol. 72, No. 9
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.9.5412-5418.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Identification of a Polyclonal B-Cell Activator in Plasmodium falciparum

Daria Donati,1,2,{dagger} Li Ping Zhang,1,{dagger} Qijun Chen,1,3 Arnaud Chêne,1,2 Kirsten Flick,1,3 Maja Nyström,1 Mats Wahlgren,1,3 and Maria Teresa Bejarano1,2*

Microbiology and Tumorbiology Center, Karolinska Institutet,1 Center for Infectious Medicine, Karolinska Institutet, Huddinge University Hospital,2 Swedish Institute for Infectious Disease Control, Stockholm, Sweden3

Received 10 March 2003/ Returned for modification 23 May 2003/ Accepted 9 June 2004

Polyclonal B-cell activation and hypergammaglobulinemia are prominent features of human malaria. We report here that Plasmodium falciparum-infected erythrocytes directly adhere to and activate peripheral blood B cells from nonimmune donors. The infected erythrocytes employ the cysteine-rich interdomain region 1{alpha} (CIDR1{alpha}) of P. falciparum erythrocyte membrane protein 1 (PfEMP1) to interact with the B cells. Stimulation with recombinant CIDR1{alpha} induces proliferation, an increase in B-cell size, expression of activation molecules, and secretion of immunoglobulins (immunoglobulin M) and cytokines (tumor necrosis factor alpha and interleukin-6). Furthermore, CIDR1{alpha} binds to Fab and Fc fragments of human immunoglobulins and to immunoglobulins purified from the sera of different animal species. This binding pattern is similar to that of the polyclonal B-cell activator Staphylococcus aureus protein A. Our findings shed light on the understanding of the molecular basis of polyclonal B-cell activation during malaria infections. The results suggest that the var gene family encoding PfEMP1 has evolved not only to mediate the sequestration of infected erythrocytes but also to manipulate the immune system to enhance the survival of the parasite.

* Corresponding author. Mailing address: Center for Infectious Medicine (CIM), Department of Medicine, Karolinska Institutet, Huddinge University Hospital, F59, S-141 86 Stockholm, Sweden. Phone: 46 8 58581158. Fax: 46 8 7467637. E-mail: marbej{at}ki.se.

Editor: S. H. E. Kaufmann

{dagger} D.D. and L.P.Z. contributed equally to this work.

Infection and Immunity, September 2004, p. 5412-5418, Vol. 72, No. 9
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.9.5412-5418.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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