Transcriptional control of HLA-A,B,C antigen in human placental cytotrophoblast isolated using trophoblast- and HLA-specific monoclonal antibodies and the fluorescence-activated cell sorter.

Kawata, Makoto; Parnes, Jane R.; Herzenberg, L A

doi:10.1084/jem.160.3.633

Cited by 59 publications

(8 citation statements)

References 43 publications

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“…Indeed, it has been shown that mouse embryos express polymorphic MHC molecules in the second half of gestation only and at a much reduced level compared with adult tissues (David-Watines, 1990;Morello et al, 1985;Ozato et al, 1985). Moreover, and despite much earlier controversy, the weight of evidence indicates that trophectoderm-derived tissues of the placenta, at the maternal-fetal interface, are deprived of such antigens throughout gestation (Hunt et al, 1987(Hunt et al, , 1988Kawata et al, 1984;Murphy et al, 1997). Thus we started to test this hypothesis by producing transgenic mice expressing polymorphic MHC class I molecules (H-2K b ) early in embryogenesis, including at the maternal-fetal interface, and analyzing the consequences for fetal development.…”

Section: Discussionmentioning

confidence: 99%

“…Yet, in the vast majority of cases, there is no evidence for rejection, and pregnancy proceeds unimpeded until term. It has been demonstrated that the extravillous cytotrophoblast in human placenta expresses a nonpolymorphic class Ib molecule (HLA-G) at the cell surface (Kovats et al, 1990) but no polymorphic class Ia antigens (Hunt et al, 1987(Hunt et al, , 1988Kawata et al, 1984). In the mouse, class Ia molecules are expressed on embryonic cells during the second half of gestation at low levels but remain absent from the trophoblast cell surface in the placenta.…”

Section: Introductionmentioning

confidence: 99%

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Selective loss of mouse embryos due to the expression of transgenic major histocompatibility class I molecules early in embryogenesis

Aït-Azzouzene¹,

Langkopf²,

Cohen³

et al. 1998

Mol. Reprod. Dev.

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Among the numerous hypotheses proposed to explain the absence of fetal rejection by the mother in mammals, it has been suggested that regulation of expression of the polymorphic major histocompatibility complex (MHC) at the fetal‐maternal interface plays a major role. In addition to a lack of MHC gene expression in the placenta throughout gestation, the absence of polymorphic MHC molecules on the early embryo, as well as their low level of expression after midgestation, could contribute to this important biologic phenomenon. In order to test this hypothesis, we have produced transgenic mice able to express polymorphic MHC class I molecules early in embryogenesis. We have placed the MHC class Ia gene H‐2Kb under the control of a housekeeping gene promoter, the hydroxy‐methyl‐glutaryl coenzyme A reductase (HMG) gene minimal promoter. This construct has been tested for functionality after transfection into mouse fibroblast L cells. The analysis of three founder transgenic mice and their progeny suggested that fetoplacental units that could express the H‐2Kb heavy chains are unable to survive in utero beyond midgestation. We have shown further that a much higher resorption rate, on days 11 to 13 of embryonic development, is observed among transgenic embryos developing from eggs microinjected at the one‐cell stage with the pHMG‐Kb construct than in control embryos. This lethality is not due to immune phenomena, since it is observed in histocompatible combinations between mother and fetus. These results are discussed in the context of what is currently known about the regulation of MHC expression at the fetal‐maternal interface and in various transgenic mouse models. Mol. Reprod. Dev. 50:35–44, 1998. © 1998 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Selective loss of mouse embryos due to the expression of transgenic major histocompatibility class I molecules early in embryogenesis

Aït-Azzouzene¹,

Langkopf²,

Cohen³

et al. 1998

Mol. Reprod. Dev.

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“…DNA Probes. cDNA probes for the human 132m and HLA-A,B,C mRNA were as previously described (26) . A 600-bp Sac I-Kpn I genomic fragment containing exon II of the /02m gene and flanking intron sequence was used as a probe for mouse 132m (12) .…”

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confidence: 99%

Rescue of Daudi cell HLA expression by transfection of the mouse beta 2-microglobulin gene.

Seong

Clayberger

Krensky

et al. 1988

The Journal of Experimental Medicine

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The Daudi cell line is a B-lymphoblastoid line derived from a Burkitt lymphoma. Daudi cells lack cell surface expression of class I HLA molecules despite the presence of intracellular class I heavy chains. They have a defect in the gene encoding beta 2-microglobulin (beta 2m), resulting in lack of translatable mRNA for this protein. It has been thought that this deficiency is responsible for the lack of cell surface class I expression. However, data have recently been presented demonstrating that at least one mouse class I heavy chain can be expressed on the cell surface in the absence of beta 2m. These results raised the questions of whether the lack of beta 2m is the only defect in Daudi and whether transfer of this single gene could restore surface class I expression. We found that transfection of the mouse beta 2m gene into Daudi indeed rescued cell surface expression of class I HLA molecules, and that these molecules could be recognized both by monomorphic and allospecific mAbs. CTL clones specific for HLA-B17 or a determinant shared by HLA-B17 and HLA-A2 killed the Daudi cells transfected with the beta 2m gene, but not untransfected Daudi or Daudi transfected with vector alone. Mouse beta 2m on the transfected Daudi cells could exchange with human beta 2m when the cells were incubated in human serum. This exchange did not alter the ability of the cells to be killed by the specific CTLs. These results demonstrate that the lack of beta 2m is the sole reason for lack of surface class I molecules in Daudi cells, and that beta 2m is required for cell surface expression of the specific class I heavy chains of Daudi.

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“…In mid-gestation human placentae, only the interstitial (extravillous) and endovascular cytotrophoblast cells are positive for Class I (HLA-ABC) MHC antigens; villous trophoblast and syncytiotrophoblast cells are negative. [13][14][15][16] By term, Class I antigen expression on cytotrophoblast markedly declines. 17 In murine placentae, Class I (H2K and D) antigen positive cells have been located in spongiotrophoblast and fetal endothelial cells.…”

Section: Trophoblast Antigensmentioning

confidence: 99%

Maternal Immune Reactivity as a Determinant of Placental Function and Fetal Survival

Mogil¹,

Wegmann²

1988

Semin Reprod Med

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Transcriptional control of HLA-A,B,C antigen in human placental cytotrophoblast isolated using trophoblast- and HLA-specific monoclonal antibodies and the fluorescence-activated cell sorter.

Cited by 59 publications

References 43 publications

Selective loss of mouse embryos due to the expression of transgenic major histocompatibility class I molecules early in embryogenesis

Selective loss of mouse embryos due to the expression of transgenic major histocompatibility class I molecules early in embryogenesis

Rescue of Daudi cell HLA expression by transfection of the mouse beta 2-microglobulin gene.

Maternal Immune Reactivity as a Determinant of Placental Function and Fetal Survival

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