Adherence of human immunodeficiency virus-infected lymphocytes to fetal placental cells: a model of maternal --&gt; fetal transmission.

Schwartz, David H.; Sharma, Usha; Perlman, Elizabeth J.; Blakemore, Karin J.

doi:10.1073/pnas.92.4.978

Cited by 24 publications

(12 citation statements)

References 33 publications

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“…The most topical of these pathogens are the human lentiviruses, which can be transmitted in utero [27,28]. It has been suggested that fetal trophoblast cells and placental macrophages may be important components promoting intrauterine infections [29][30][31]; however, our model would support direct infection of the fetus rather than infection of the placenta.…”

Section: Discussioncontrasting

confidence: 54%

Maternal Cells are Widely Distributed in Murine Fetuses in Utero1

Piotrowski

Croy

1996

Biology of Reproduction

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Passage of maternal cells into conceptuses in utero is recognized but poorly defined in species with hemochorial placentation. Despite the potential importance for such a phenomenon in vertical disease transmission, only limited data address the frequency of material to fetal cell trafficking or the developmental stage of its initiation. A murine model system, involving transfer of LacZ-, scid/scid, or wild type (+/+) blastocysts to pseudo-pregnant, LacZ+ transgenic ROSA26 females provided both flow cytometric and in situ information. In 100% of the late-gestation pregnancies studied, nucleated LacZ+ maternal cells crossed to conceptuses. In 90% of scid/scid fetuses, nucleated maternal cells were present in at least one lymphoid organ and often in more than one organ. Thymus was the most frequent site for maternal cell detection while the highest proportions of maternal cells were found in liver. Maternal cells were also visualized in fetal lung, heart, and bone marrow. Maternal cell trafficking into scid/scid fetuses commenced about midgestation, coincident with maturation of a placental circulation. In late-gestation +/+ fetuses, maternal cells were found extensively throughout bone marrow but not in other organs. The presence of maternal cells within primary lymphoid organs of fetuses may influence the repertoire of the developing fetal immune system and may be an underappreciated mechanism for vertical disease transmission.

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Section: Discussioncontrasting

confidence: 54%

Maternal Cells are Widely Distributed in Murine Fetuses in Utero1

Piotrowski

Croy

1996

Biology of Reproduction

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“…The transmission of maternal cells could also be responsible for the vertical transfer of infectious agents, such as HIV-1 [23,24]. The transfer of a natural killer-cell lymphoma from mother to fetus has also been described [25].…”

Section: Introductionmentioning

confidence: 96%

Affinity-Dependent Alterations of Mouse B Cell Development by Noninherited Maternal Antigen1

Vernochet¹,

Caucheteux²,

Gendron³

et al. 2005

Biology of Reproduction

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We have examined the passage of maternal cells into the fetus during the gestation and postpartum in mice. Using enhanced green fluorescent protein (EGFP)-transgenic females, we showed that maternal cells frequently gain access to the fetus, mostly in syngeneic pregnancies, but also in allogeneic and outbred crosses. EGFP-transgenic cells, including B, T, and natural killer cells, can persist until adulthood, primarily in bone marrow and thymus. We then asked whether maternal cells, bearing antigens not inherited by the fetus, influence the development of fetal and neonatal B lymphocytes. We have used the B cell receptor 3-83 mu/delta transgenic mouse model, whose B cells recognize the major histocompatibility complex class I molecules H-2Kk and H-2Kb, with a high or moderate affinity, respectively. The fate of transgenic B cells in animals exposed to noninherited H-2Kk or H-2Kb maternal antigens (NIMA) during gestation and lactation was compared with those of nonexposed controls. In H-2Kk-exposed fetuses, NIMA-specific transgenic B cells are partially deleted during late gestation. Nondeleted cells have downmodulated their B cell receptor. In contrast, in NIMA H-2Kb-exposed neonates, transgenic B cells present an activated phenotype, including proliferation, upregulation of surface CD69, and preferential localization in the T cell zone of splenic follicles. This state of activation is still clearly detectable up to 3 wk of age. Thus, we show that fetal and neonatal B cell development is affected by maternal cells bearing antigens noninherited by the fetus and that this phenomenon is highly dependent on the affinity of the B cell receptor for the NIMA.

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“…It appears that the phe notype of the virus and the type of the cell involved in such assays may deviate from the expected outcome into the opposite direction as human antibodies which were effective in vitro were not capable of neutralizing the same virus in vivo [47], Despite the progress in anti-HIV vaccine development, very little is known about the pro tective effects of neutralizing Abs against the spread of HIV to the tissues outside of the blood compartment. Schwartz et al [48] suggested recently that polyclonal Abs and soluble CD4 can block cell-mediated HIV infection in chorionic villus cultures. However, these primary cul tures consisted of mesenchymal fibroblastoid cells located beneath the trophoblast layer, which constitutes the outer surface of the placenta.…”

Section: Failure Of Hiv Antibodies To Protect Placental Trophoblastsmentioning

confidence: 99%

Failure of Neutralizing gp120 Monoclonal Antibodies to Prevent HIV Infection of Choriocarcinoma-Derived Trophoblasts

Bourinbaiar¹,

Borkowsky²,

Krasinski³

et al. 1997

J Biomed Sci

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Although placental trophoblasts, the only fetal cells in direct contact with infectious maternal blood, can be infected with HIV, the precise cause for the low transmission rate of virus across the placental barrier is unknown. One of the most common conjectures is that maternal anti- HIV antibodies (Abs) contribute to the protection of the fetus. This hypothesis has been tested in vitro by infecting the CD4-negative placental trophoblast line, BeWo, with HIV-1 mg in the presence of serial dilutions of neutralizing monoclonal Abs against the V3 loop (No. 694) or CD4-bindmg conformational domain (No. 588). The results, based on measurement of p24 production from virus-exposed cells, reveal that the titers of Abs, adequate in preventing the infection of control MT-4 T lymphocytes, were less effective in protecting trophoblasts. Furthermore, PCR analysis of HIV DNA formed after a single round of infection has shown no significant decrease in the number of viral copies in Ab-protected BeWo cells. An anti-HIV serum from a pregnant woman did also have no effect. Although our in vitro observations do not necessarily apply to the in vivo situation, the results suggest that the humoral immune response sustained by neutralizing Abs may be able to protect T lymphocytes, but not placental trophoblasts. The findings are consistent with recent clinical studies demonstrating a lack of correlation between the presence of neutralizing anti-HIV Abs in pregnant women and HIV transmission in utero.

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Adherence of human immunodeficiency virus-infected lymphocytes to fetal placental cells: a model of maternal --> fetal transmission.

Cited by 24 publications

References 33 publications

Maternal Cells are Widely Distributed in Murine Fetuses in Utero1

Maternal Cells are Widely Distributed in Murine Fetuses in Utero1

Affinity-Dependent Alterations of Mouse B Cell Development by Noninherited Maternal Antigen1

Failure of Neutralizing gp120 Monoclonal Antibodies to Prevent HIV Infection of Choriocarcinoma-Derived Trophoblasts

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