Present addresses: Centre de Recherche Biomoléculaire Pietro Annigoni (CERBA), Burkina Faso.
Plasmodium falciparum infection of the placenta impacts on the T helper type 1 (Th1)/Th2 balance of neonatal T cells through CD4+CD25+ forkhead box P3+ regulatory T cells and interleukin-10
Article first published online: 17 AUG 2009
© 2009 British Society for Immunology
Clinical & Experimental Immunology
Volume 158, Issue 3, pages 287–293, December 2009
How to Cite
Bisseye, C., Van Der Sande, M., Morgan, W. D., Holder, A. A., Pinder, M. and Ismaili, J. (2009), Plasmodium falciparum infection of the placenta impacts on the T helper type 1 (Th1)/Th2 balance of neonatal T cells through CD4+CD25+ forkhead box P3+ regulatory T cells and interleukin-10. Clinical & Experimental Immunology, 158: 287–293. doi: 10.1111/j.1365-2249.2009.04014.x
- Issue published online: 29 OCT 2009
- Article first published online: 17 AUG 2009
- Accepted for publication 6 August 2009
- placental malaria;
Placental malaria infection affects the T helper type 1 (Th1)/Th2 balance in neonatal children. We investigated a potential role of regulatory T cells in this balance by comparing T cell responses of cord blood mononuclear cells (CBMC) from parasitized and non-parasitized placenta of Gambian women. CBMC were depleted of CD4+CD25+ forkhead box P3 (FoxP3)+ regulatory T cells and analysed in vitro for their ability to produce interferon (IFN)-γ, sCD30 and interleukin (IL)-10 in response to phytohaemagglutinin (PHA), live Plasmodium falciparum, schizont extracts and the recombinant P. falciparum blood stage antigen merozoite surface protein 1 (MSP119). As expected, lower IFN-γ and higher sCD30 responses were observed for the cells from the parasitized group. In addition, higher IL-10 levels were produced by CBMC from the parasitized group. Depletion of regulatory T cells decreased IL-10 production, which resulted in a restoration of IFN-γ expression in response to all stimuli. The Th2 marker sCD30 remained significantly higher in the parasitized group in response to malaria protein antigens while similar levels were recovered between both groups in response to live P. falciparum. Similar effects were observed by adding an antibody that blocks IL-10 function. These results suggest that the impact of P. falciparum infection on Th1 differentiation of neonatal T cells can be ascribed to regulatory T cells through production of IL-10.