Co-ordinate expression of Th1/Th2 phenotypes in maternal and fetal blood: evidence for a transplacental nexus.
If maternal atopy and environmental exposure affect prenatal Th cell development, the maternal and fetal immune systems should display common Th1/Th2 phenotypes. To test this hypothesis, we studied maternal and neonatal blood samples from mothers with total serum IgE <300 IU/mL. Basal levels of IFN-γ, IL-4, and eotaxin in paired maternal and fetal sera were tightly correlated. Polyclonal T cell activation in vitro by Staphylococcal exotoxin B induced co-ordinate IFN-γ production from paired maternal and fetal mononuclear cells, accompanied by co-ordinate increases in activated CD4+CD69+ cells that display the CCR4+Th2 and CXCR3+ Th1 phenotypes. Maternal and fetal CD4+CXCR3+ T cells were subsequently identified as the major producers of IFN-γ. The data established that a transplacental nexus exists during normal pregnancy and that fetal Th cell responses may be biased by the maternal immune system.
Division of Infectious Disease and Immunology, Department of Medicine, New York University School of Medicine, New York, NY, USA.
Doris B
DB
Tse
Bruce K
BK
Young
D015496:CD4-Positive T-Lymphocytes / Q000737:chemistry / Q000276:immunology; D054413:Chemokine CCL11; D005260:Female; D005312:Fetal Blood / Q000737:chemistry / Q000166:cytology* / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007231:Infant, Newborn; D007371:Interferon-gamma / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D008213:Lymphocyte Activation; D010641:Phenotype; D011247:Pregnancy; D054397:Receptors, CCR3 / Q000032:analysis; D054398:Receptors, CCR4 / Q000032:analysis; D018417:Th1 Cells / Q000737:chemistry / Q000276:immunology*; D018418:Th2 Cells / Q000737:chemistry / Q000276:immunology*
D054413:Chemokine CCL11; D054397:Receptors, CCR3; D054398:Receptors, CCR4; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma