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 pathway

Francis M. Ndungu, Latifu Sanni, Britta Urban, Robin Stephens, Christopher I. Newbold, Kevin Marsh, Jean Langhorne

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

We have studied the human CD4 T cell response to a functionally conserved domain of Plasmodium falciparum erythrocyte membrane protein-1, cysteine interdomain region-1α (CIDR-1α). Responses to CIDR-1α were striking in that both exposed and nonexposed donors responded. The IFN-γ response to CIDR-1α in the nonexposed donors was partially independent of TCR engagement of MHC class II and peptide. Contrastingly, CD4 T cell and IFN-γ responses in malaria-exposed donors were MHC class II restricted, suggesting that the CD4 T cell response to CIDR-1α 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-1α 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-1α 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 languageEnglish (US)
Pages (from-to)5504-5512
Number of pages9
JournalJournal of Immunology
Volume176
Issue number9
StatePublished - May 1 2006
Externally publishedYes

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Malaria
Cysteine
T-Lymphocytes
Plasmodium falciparum
Interleukin-12
Interleukin-10
Dendritic Cells
Interleukin-18
Cell Communication
Plasmodium falciparum erythrocyte membrane protein 1
Erythrocytes
Cytokines
Peptides

ASJC Scopus subject areas

  • Immunology

Cite this

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 pathway. / Ndungu, Francis M.; Sanni, Latifu; Urban, Britta; Stephens, Robin; Newbold, Christopher I.; Marsh, Kevin; Langhorne, Jean.

In: Journal of Immunology, Vol. 176, No. 9, 01.05.2006, p. 5504-5512.

Research output: Contribution to journalArticle

Ndungu, Francis M. ; Sanni, Latifu ; Urban, Britta ; Stephens, Robin ; Newbold, Christopher I. ; Marsh, Kevin ; Langhorne, Jean. / 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 pathway. In: Journal of Immunology. 2006 ; Vol. 176, No. 9. pp. 5504-5512.
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abstract = "We have studied the human CD4 T cell response to a functionally conserved domain of Plasmodium falciparum erythrocyte membrane protein-1, cysteine interdomain region-1α (CIDR-1α). Responses to CIDR-1α were striking in that both exposed and nonexposed donors responded. The IFN-γ response to CIDR-1α in the nonexposed donors was partially independent of TCR engagement of MHC class II and peptide. Contrastingly, CD4 T cell and IFN-γ responses in malaria-exposed donors were MHC class II restricted, suggesting that the CD4 T cell response to CIDR-1α 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-1α 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-1α 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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