title: Activation status of cord blood gamma delta T cells reflects in utero exposure to Plasmodium falciparum antigen.
abstract: BACKGROUND
  Placental Plasmodium falciparum infection modulates neonatal cell-mediated immune responses and is associated with increased susceptibility of infants to malaria.
  
  
  METHODS
  By flow-cytometric analysis of maternal peripheral and cord blood samples collected at delivery, we measured and compared the activation status and proinflammatory cytokine activity of T cells from women segregated into groups according to malaria status.
  
  
  RESULTS
  Stimulation with phorbol myristate acetate/ionomycin resulted in the highest percentages of tumor necrosis factor-alpha- and interferon-gamma-positive gamma delta T cells in peripheral blood samples and in corresponding cord blood samples from those treated for malaria during pregnancy. Cord blood samples from this group also contained significantly higher percentages of CD69(+) and CD25(+) gamma delta T cells and CD3(+) T cells, compared with samples from either the group with active placental P. falciparum infection at delivery or the group with no infection. Proinflammatory cytokine activity of cells from the group with placental P. falciparum infection at delivery was either similar to or lower than that of cells from the group with no infection.
  
  
  CONCLUSIONS
  The findings imply that treatment of P. falciparum malaria during pregnancy leads to enhanced innate immune T cell activation and proinflammatory cytokine responses in both maternal and fetal compartments. Ongoing placental P. falciparum infection, conversely, is associated with an absence of such activity.
authors.affiliation: Department of Parasitology, Institute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
authors.forename: Ilka
authors.initials: I
authors.lastname: Engelmann
authors.forename: Andrea
authors.initials: A
authors.lastname: Santamaria
authors.forename: Peter G
authors.initials: PG
authors.lastname: Kremsner
authors.forename: Adrian J F
authors.initials: AJ
authors.lastname: Luty
mesh_terms: D000293:Adolescent; D000328:Adult; D000818:Animals; D015703:Antigens, CD / Q000502:physiology; D000945:Antigens, Differentiation, T-Lymphocyte / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D005260:Female; D005312:Fetal Blood / Q000166:cytology / Q000276:immunology*; D015870:Gene Expression; D006801:Humans; D037181:Lectins, C-Type; D008213:Lymphocyte Activation / Q000502:physiology*; D016778:Malaria, Falciparum / Q000276:immunology*; D011247:Pregnancy; D015597:Pregnancy Complications, Parasitic / Q000276:immunology*; D015375:Receptors, Interleukin-2 / Q000502:physiology; D016176:T-Lymphocyte Subsets / Q000502:physiology*; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D016207:Cytokines; D037181:Lectins, C-Type; D015375:Receptors, Interleukin-2; D000099192:CD69 Antigens