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Infection and Immunity, July 2004, p. 4233-4239, Vol. 72, No. 7
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.7.4233-4239.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Response of the Splenic Dendritic Cell Population to Malaria Infection

Andrew L. Leisewitz,1,2,3* Kirk A. Rockett,1,2 Bonginkosi Gumede,1,2,4 Margaret Jones,5 Britta Urban,1,6 and Dominic P. Kwiatkowski1,2

Weatherall Institute of Molecular Medicine,1 Nuffield Department of Clinical Laboratory Sciences,5 Nuffield Department of Clinical Medicine, University of Oxford,6 University Department of Paediatrics, John Radcliffe Hospital, Oxford, United Kingdom,2 Companion Animal Clinical Studies, University of Pretoria, Pretoria,3 Department of Pharmacology, University of Cape Town, Cape Town, South Africa4

Received 9 September 2003/ Returned for modification 28 October 2003/ Accepted 28 February 2004

Dendritic cells, particularly those residing in the spleen, are thought to orchestrate acquired immunity to malaria, but it is not known how the splenic dendritic cell population responds to malaria infection and how this response compares with the responses of other antigen-presenting cells. We investigated this question for Plasmodium chabaudi AS infection in C57BL/6 mice. We found that dendritic cells, defined here by the CD11c marker, migrated from the marginal zone of the spleen into the CD4+ T-cell area within 5 days after parasites entered the bloodstream. This contrasted with the results observed for the macrophage and B-cell populations, which expanded greatly but did not show any comparable migration. Over the same time period dendritic cells showed upregulation of CD40, CD54, and CD86 costimulatory molecules that are required for successful T-cell activation. In dendritic cells, the peak intracellular gamma interferon expression (as shown by fluorescence-activated cell sorting) was on day 5, 2 days earlier than the peak expression in B-cells or macrophages. These findings show that splenic dendritic cells are actively engaged in the earliest phase of malarial infection in vivo and are likely to be critical in shaping the subsequent immune response.

* Corresponding author. Mailing address: Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria, Private Bag X04, Onderstepoort, 0110, South Africa. Phone: 27 12 529 8278. Fax: 27 12 529 8308. E-mail: andrew.leisewitz{at}up.ac.za.

Editor: J. F. Urban, Jr.

Infection and Immunity, July 2004, p. 4233-4239, Vol. 72, No. 7
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.7.4233-4239.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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