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We have studied the human CD4 T cell response to a functionally conserved domain of Plasmodium falciparum erythrocyte membrane protein-1, cysteine interdomain region-1alpha (CIDR-1alpha). Responses to CIDR-1alpha were striking in that both exposed and nonexposed donors responded. The IFN-gamma response to CIDR-1alpha in the nonexposed donors was partially independent of TCR engagement of MHC class II and peptide. Contrastingly, CD4 T cell and IFN-gamma responses in malaria-exposed donors were MHC class II restricted, suggesting that the CD4 T cell response to CIDR-1alpha 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-1alpha 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-1alpha and the host cell may be responsible for regulation of the CD4 T cell and cytokine responses to P. falciparum-infected erythrocytes reported previously.

Original publication




Journal article


J Immunol

Publication Date





5504 - 5512


Adult, Animals, Antigens, CD, Antigens, Differentiation, T-Lymphocyte, CD36 Antigens, CD4-Positive T-Lymphocytes, Cell Division, Cells, Cultured, Cysteine, Dendritic Cells, Histocompatibility Antigens Class II, Humans, Interferon-gamma, Killer Cells, Natural, Lectins, C-Type, Malaria, Plasmodium falciparum, Protein Binding, Protozoan Proteins, Receptors, Antigen, T-Cell