Plasmodium falciparum induces a Th1/Th2 disequilibrium, favoring the Th1-type pathway, in the human placenta /Fievet, Nadine Moussa, M. Tami, G. Maubert, B. /Cot, Michel Deloron, P. Chaouat, G. PALUDISME AGENT PATHOGENE FEMME GROSSESSE IMMUNITE IMMUNOLOGIE CELLULE CULTURE IN VITRO ETUDE EXPERIMENTALE TRANSMISSION PLACENTAIRE TH1 CYTOKINE TH2 CYTOKINE During pregnancy, a local and systemic Th2 bias of maternal immunity favors Th1-dependent infections such as malaria. This study measured cytokines secreted in cultures of chorionic villi, placental blood cells (PBC), and serum in term placentas from 88 malaria-infected and -noninfected Cameroon women. Interleukin (IL)-2 and-4 were consistently low ; IL-1Beta, IL-6, granulocyte-macrophage colony-stimulating factor, and transforming growth factor (TGF)-Beta2 were highest in PBC cultures. Malaria placental infection increased Th1-type cytokines, whereas Th-type cytokines and TGF-Beta2 were unchanged. Addition of lipopolysaccharide or infected erythrocytes to cultures increased TNF-alpha, IL-1Beta, IL-6,and IL-10 secretions but not those of IFN-gamma and IL-4. Overall, Plasmodium falciparum induced a placental immune response involving both Th1- and Th2-type cell activation. Although the Th1 pathway was favored, IL-10 secretion was also increased, and this increase should be effective in protecting the placenta by controlling the negative effects of Th1 cytokines on pregnancy. (Résumé d'auteur) 2001 text https://www.documentation.ird.fr/hor/fdi:010025993 fdi:010025993 Fievet Nadine, Moussa M., Tami G., Maubert B., Cot Michel, Deloron P., Chaouat G.. Plasmodium falciparum induces a Th1/Th2 disequilibrium, favoring the Th1-type pathway, in the human placenta. 2001, 183 (10), 1530-1534 EN CAMEROUN YAOUNDE