Human parvovirus B19 can cause congenital infection with variable morbidity and mortality in the fetus and neonate. Although much information exists on the B19-specific antibody response in pregnant women, little information is available describing the cell-mediated immune (CMI) response at the maternal-fetal interface. The focus of this study was to characterize the CMI response within placentas from women who seroconverted to B19 during their pregnancies and compare it to controls. Immunohistochemical techniques were used to identify the various immune cells and the inflammatory cytokine present within placental tissue sections. Group 1 consisted of placentas from 25 women whose pregnancies were complicated by B19 infection; 6 women with good outcome (near-term or term delivery), and 19 with poor outcome (spontaneous abortion, nonimmune hydrops fetalis, or fetal death). Group 2 consisted of placentas from 20 women whose pregnancies were complicated with nonimmune hydrops fetalis of known, noninfectious etiology. Group 3 consisted of placentas from eight women whose pregnancies ended in either term delivery or elective abortion. The results of the study revealed a statistically significant increase in the number of CD3-positive T cells present within placentas from group 1 compared to group 2 or 3 (13.3 versus 2 and 1, respectively) (P < 0.001). In addition, the inflammatory cytokine interleukin 2 was detected in every placenta within group 1 but was absent from all placentas evaluated from groups 2 and 3. Together, these findings demonstrate evidence for an inflammation-mediated cellular immune response within placentas from women whose pregnancies are complicated with B19 infection.The placenta plays an integral barrier role in limiting congenital viral infections (18). However, some viruses, transmitted via the blood, are able to circumvent this barrier. Virus within maternal blood reaches the intervillous space and makes intimate contact with the placental trophoblast layer, which can lead to virus transmission across that protective barrier to the fetal side. Transmission can occur through breaks in the placental barrier, via endocytosis or receptormediated transfer.The P blood group antigen globoside is the main cellular receptor for B19 (3,4). Globoside is present not only on cells of the erythroid lineage but also on the surface of placental syncytiotrophoblast and cytotrophoblast cells (17). The presence of the globoside receptor on trophoblast cells may play a role in transmission of the virus across the placenta.B19 infection of pregnant women can lead to vertical transmission of virus to the fetus with outcomes that include spontaneous abortion, fetal anemia, nonimmune hydrops fetalis, and intrauterine fetal death (6,15,23,26,31,36). Although B19 is capable of causing congenital infection, numerous clinical studies show clearly that the majority of women who become infected with B19 during pregnancy deliver healthy infants (9,20,27,29,37). The risk of fetal demise appears to be greatest when infecti...