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CD4 T Cells from Malaria-Nonexposed Individuals Respond to the CD36-Binding Domain of Plasmodium falciparum Erythrocyte Membrane Protein-1 via an MHC Class II-TCR-Independent Pathway¹

Francis M. Ndungu^*,, Latifu Sanni^*,, Britta Urban, Robin Stephens^*, Christopher I. Newbold^¶, Kevin Marsh and Jean Langhorne^2,*

^* Division of Parasitology, National Institute for Medical Research, London, United Kingdom; Kenya Medical Research Institute, Centre for Geographic Medicine Research, Kilifi, Kenya; Department of Pathology, Leeds General Infirmary, Leeds, United Kingdom; Nuffield Department of Clinical Medicine, Centre for Clinical Vaccinology and Tropical Medicine, University of Oxford, Oxford, United Kingdom; and ^¶ Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom

We have studied the human CD4 T cell response to a functionally conserved domain of Plasmodium falciparum erythrocyte membrane protein-1, cysteine interdomain region-1 (CIDR-1). Responses to CIDR-1 were striking in that both exposed and nonexposed donors responded. The IFN- response to CIDR-1 in the nonexposed donors was partially independent of TCR engagement of MHC class II and peptide. Contrastingly, CD4 T cell and IFN- responses in malaria-exposed donors were MHC class II restricted, suggesting that the CD4 T cell response to CIDR-1 in malaria semi-immune adults also has a TCR-mediated component, which may represent a memory response. Dendritic cells isolated from human peripheral blood were activated by CIDR-1 to produce IL-12, IL-10, and IL-18. IL-12 was detectable only between 6 and 12 h of culture, whereas the IL-10 continued to increase throughout the 24-h time course. These data strengthen previous observations that P. falciparum interacts directly with human dendritic cells, and suggests that the interaction between CIDR-1 and the host cell may be responsible for regulation of the CD4 T cell and cytokine responses to P. falciparum-infected erythrocytes reported previously.

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The JI 2006 176: 5131-5132. [Full Text]  

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