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Infection and Immunity, October 2006, p. 5725-5729, Vol. 74, No. 10
0019-9567/06/$08.00+0 doi:10.1128/IAI.00682-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Rolf Fendel,1,2
Benjamin Mordmueller,1,2
Ayola A. Adegnika,1,2,3
Peter G. Kremsner,1,2 and
Adrian J. F. Luty1,2*
Medical Research Unit, Albert Schweitzer Hospital, Lambaréné, Gabon,1 Institute for Tropical Medicine, Department of Parasitology, University of Tübingen, Tübingen, Germany,2 Department of Parasitology, Leiden University Medical Centre, Leiden, The Netherlands3
Received 28 April 2006/ Returned for modification 31 May 2006/ Accepted 7 July 2006
Placental Plasmodium falciparum infection affects birth outcomes and sensitizes fetal lymphocytes to parasite antigens. We assessed the influence of maternal P. falciparum infection on fetal myeloid dendritic cells (mDC) and plasmacytoid dendritic cells (pDC), analyzing the cord blood of offspring of Gabonese mothers with different infection histories. Cord blood from newborns of mothers with malarial infection at delivery had significantly more mDC than that from nonexposed newborns (P = 0.028) but mDC and pDC HLA-DR expression was unrelated to maternal infection history. Independently of these findings, cord blood mDC and pDC numbers declined significantly as a function of increasing maternal age (P = 0.029 and P = 0.033, respectively). The inducible antigen-specific interleukin-10-producing regulatory-type T-cell population that we have previously detected in cord blood of newborns with prolonged in utero exposure to P. falciparum may directly reflect the altered DC numbers in such neonates, while the maintenance of cord blood DC HLA-DR expression contrasts with that of DC from P. falciparum malaria patients.
Present address: Research Institute of Integrative and Comparative Biology, University of Leeds, Leeds, United Kingdom.
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