The Journal of Experimental Medicine
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Published online 5 June 2006 doi:10.1084/jem.20052450
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 6, 1427-1433
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BRIEF DEFINITIVE REPORT

 Malaria infection changes the ability of splenic dendritic cell populations to stimulate antigen-specific T cells

Anne-Marit Sponaas1, Emma Tamsin Cadman1, Cecile Voisine1, Vicky Harrison1, Andre Boonstra2, Anne O'Garra2, and Jean Langhorne1

1 Division of Parasitology and 2 Division of Immunoregulation, National Institute for Medical Research, London NW7 1AA, United Kingdom

CORRESPONDENCE J. Langhorne: jlangho{at}nimr.mrc.ac.uk

The capacity of splenic CD11c+ dendritic cell (DC) populations to present antigen (Ag) to T cells differs during malarial infection with Plasmodium chabaudi in mice. Both CD11c+CD8+ and CD8– DCs presented malarial peptides on their surface during infection. However, although both DC subsets expressing malaria peptides could induce interferon-{gamma} production by CD4 T cells, only CD8– DCs isolated at the acute phase of infection stimulated Ag-specific T cell proliferation and interleukin (IL)-4 and -10 production from MSP1-specific T cell receptor for Ag transgenic T cells coincidental with our reported Th1 to Th2 switch at this stage in response to the pathogen. The timing of these distinct DC responses coincided with increased levels of apoptosis in the CD8+ population and an increase in the numbers of CD8– DCs in the spleen. Our data suggest that the switch in CD4 T cell responses observed in P. chabaudi–infected mice may be the result of the presentation by different DC populations modified by the malaria infection.


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