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Infection and Immunity, April 2001, p. 2364-2371, Vol. 69, No. 4
Department of Paediatrics, Oxford University,
Oxford OX3 9DU, United Kingdom
Received 17 July 2000/Returned for modification 6 September
2000/Accepted 4 January 2001
Uncertainty remains about the cellular origins of the earliest
phase of the proinflammatory cytokine response to malaria. Here we show
by fluorescence-activated cell sorter analysis that
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.4.2364-2371.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Cellular Basis of Early Cytokine Response to
Plasmodium falciparum

T cells and
CD14+ cells from nonimmune donors produce tumor necrosis
factor and that 
T cells also produce gamma interferon within 18 h of contact with mycoplasma-free Plasmodium
falciparum-infected erythrocytes in vitro. This early cytokine
response is more effectively induced by intact than by lysed
parasitized erythrocytes. However, the IFN-
response to lysed
parasites is considerably enhanced several days after peripheral blood
mononuclear cells are primed with low numbers of intact parasitized
erythrocytes, and in this case it derives from both 
and 
T
cells. These data show that naïve 
T cells can respond
very rapidly to malaria infection but that malaria fever may involve a
multistage process in which the priming of both 
and 
T-cell populations boosts the cytokine response to lysed parasite
products released at schizont rupture.
*
Corresponding author. Mailing address: Department of
Paediatrics, John Radcliffe Hospital, Oxford University, Oxford OX3
9DU, United Kingdom. Phone: (01865) 221071. Fax: (01865) 220479. E-mail: dominic.kwiatkowski{at}paediatrics.ox.ac.uk.
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