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At least 19 recordsLinked to original sources
PubMed2026

Trophoblast Enrichment by Maternal Immune-Cell Depletion Using CD45 and CD56 Surface Markers in Trophoblast Retrieval and Isolation from the Cervix (TRIC).

Background: Trophoblast retrieval and isolation from the cervix (TRIC) has emerged as a promising alternative to invasive prenatal diagnostic procedures. However, contamination by maternal immune cells remains a major challenge that may compromise trophoblast purity and the reliability of downstream fetal genetic analyses. Methods: Maternal immune cells were selectively depleted by immunomagnetic sorting using antibodies targeting CD45 or CD56. The remaining cells were subsequently enriched for HLA-G-positive trophoblasts and characterized by immunofluorescence and gene-expression analyses using CD45, CD56, HLA-G, cytokeratin 7 (CK7), and β-human chorionic gonadotropin (β-hCG). Results: Compared with CD45-mediated depletion, CD56-mediated depletion demonstrated more efficient removal of maternal immune cells, as indicated by significantly reduced CD56 expression. CK7 expression showed an increasing trend following CD56 depletion, whereas β-hCG expression remained largely unchanged. Immunofluorescence analysis further demonstrated a significant increase in the proportion of CK7+/β-hCG+ trophoblast cells after CD56 depletion. Conclusions: Among the evaluated depletion strategies, CD56-mediated depletion demonstrated a more favorable profile for trophoblast-associated characteristics than CD45-mediated depletion, suggesting its potential contribution to further methodological optimization of trophoblast isolation in TRIC-based noninvasive prenatal genetic testing.

maternal immune cell↗
PubMed1976

Natural mechanisms of controlling lymphotropic herpesvirus infection (Marek's disease) in the chicken.

Four categories of natural resistance phenomena against Mareks disease in chickens, i.e., maternal antibody, age resistance, genetic resistance, and natural immunization, are described. In nature, these forms of resistance probably act in concert through comlex interrelationships. The mechanisms are not well understood but include humoral immunity (maternal antibody), cell-mediated immunity, and possibly other mechanisms. The possible role of newly discovered tumor-specific antigens in cell-mediated immunity against Marek's disease lymphomas is discussed.

Age Factors↗
PubMed2026

Placental Site Trophoblastic Tumor Acquires Immune Functions by Incorporating Host Maternal Genes.

Although it was proposed that cell fusion of cancer cells with leukocytes creates mobile hybrids with a metastatic phenotype, it has been difficult to genetically confirm cell fusion events in human cancer in vivo. Here, we experienced 4 cases of placental site trophoblastic tumor (PSTT) that produced immunoglobulin (Ig). Three cases showed recurrence and responded well to pembrolizumab therapy. Among them, we could analyze temporal changes in the genetic profiles on one case of daughter-derived PSTT, which relapsed after pembrolizumab therapy. In this case, we found that PSTT incorporated the exogenous genes from host maternal cells. The rearrangement patterns of Ig genes and protein expressions sequentially increased. By analyzing single-nucleotide variants, PSTT incorporated daughter-non-inherited maternal alleles (DNIMA), including the Ig lambda and HLA-DQA2 loci. Protein expressions of TLR10 and SIGLEC10 increased during tumor progression concomitantly with DNIMA incorporation. DNIMA mapping indicates the incorporation of exogenous maternal genes was widely distributed through the whole chromosomes, suggesting the involvement of cell fusion in gene transfer mechanisms. These findings indicate that PSTT sequentially incorporated exogenous genes from maternal cells to express immune-related molecules and suggest that cancer cells acquired B cell-related functions, including Ig production by cell fusion with host immune cells.

Humans↗
PubMed1979

In vitro stimulation of human colostral lymphocytes by cytomegalovirus.

Lymphocytes isolated from the peripheral blood and colostrum of 17 healthy donors, 1 to 3 days post partum, were cultured with cytomegalovirus (CMV), strain AD169, as stimulating antigen in a lymphocyte transformation test. The test was performed in microculture utilizing the cell-free supernatant of CMV-infected human fibroblasts and isolated peripheral blood and colostral lymphocytes showing normal reactivity to phytohemagglutinin. Lymphocytes from CMV-seropositive donors were stimulated by the CMV antigen, whereas lymphocytes from both male and female CMV-seronegative donors failed to respond, as measured by incorporation of tritiated thymidine. In those donors from whom utilizable colostrum samples were obtained, two donors lacking peripheral blood lymphocyte (PBL) CMV reactivity also lacked colostral lymphocyte CMV reactivity. The remaining five colostrum donors showed both PBL and colostral lymphocyte reactivity to the CMV antigen, with colostral lymphocyte reactivity in four of five donors exceeding PBL-cytomegalovirus reactivity. There was no clear-cut correlation between the titer of CMV antibody by complement fixation and the amount of tritiated thymidine incorporated into the lymphocytes stimulated with the CMV antigen. These results highlight current knowledge that milk and colostrum contain large numbers of specifically sensitized T-lymphocytes, expressing a selective quota of maternal cell-mediated immunities. We are currently investigating the possibility that CMV-reactive colostral lymphocytes obtained during suckling may be of some protective value to the immunologically inexperienced neonate by transferring an adoptive immunity. This assumes special significance in the light of known transmission of CMV via mothers' milk to neonates.

Antigens, Viral↗
PubMed1978

Inhibition of cell-mediated microcytotoxicity and stimulation of mixed lymphocyte reactivity by mouse pregnancy serum.

Blocking activity of mouse pregnancy serum was investigated using a well defined one-way mixed lymphocyte culture and a cell-mediated microcytotoxicity test. Allogeneic (C57BL (H-2b) X CBA/Ca (H-2k)) and syngeneic (C57BL (H-2b) X C57BL (H-2b)) pregnancy and postpartum sera were found to stimulate rather than inhibit the mixed lymphocyte response. In contrast, the same sera were able to abrogate target cell killing by hyperimmune lymphocytes in a cell-mediated microcytotoxicity test. Although inhibitory activity was present in both allogeneic and syngeneic 18-day pregnancy sera, indicating a non-specific effect, only allogeneic postpartum sera had significant blocking activity when compared with either the equivalent syngeneic group or the normal serum control. The specificity implied by this gained support from preliminary third-party experiments. Blocking activity was found in primiparous as well as multiparous sera. These results provide further evidence for the existence of maternal serum-blocking factors which may operate to protect the conceptus against maternal cell-mediated immunity during pregnancy, and indicate that they may act at the efferent rather than the afferent phase of the immune response.

Animals↗
PubMedDate not supplied

Antagonistic maternal immune reactions (rejection and facilitation) to the embryo in the urodele amphibian Salamandra salamandra lin.

In vitro assays have been employed to demonstrate that pregnant salamanders mount an immune reaction against their embryos. Maternal spleen cells kill up to 85% of dissociated embryonic epidermal cells during a 48 h incubation period. The degree of killing depends upon the ratio of maternal to embryonic cells and on the number of embryos borne by the mother. The cytotoxicity shows considerable specificity for the embryos of a given mother although a weak degree of killing can occur with embryos from other mothers, presumably due to some form of cross-reactivity. The effect is inhibited by the addition of maternal serum to the cultures. The degree of protection is also a function of the number of embryos borne by the mother. Pre-incubation experiments indicate that the maternal serum has a protective action on the embryonic cells which is largely specific for the female's own embryos (and suggested to be antibody in nature) and an inhibitory action on the maternal spleen cells which occurs also with spleen cells of other females (and suggested to be either an immune complex or a nonimmunological substances). An increase in beta protein peaks is seen following electrophoresis of sera from pregnant (and also allografted) salamanders. These findings indicate that the pregnant salamander mounts a double immune reaction against her embryos, an aggressive (rejection) reaction and a protective (facilitation) reaction.

Absorption↗
PubMed1978

Maternal alloimmunisation in pregnancy. In vitro studies of T cell-dependent immunity to paternal alloantigens.

A secondary in vitro allograft reaction was used to demonstrate that spleen cells derived from allogeneically mated inbred mice were immunised against paternal alloantigens. In addition to the heightened alloantigen-specific in vitro response of these spleen cells, it was also found that spleen cells froma a wide variety of syngeneically and allogeneically mated mice were nonspecifically more reactive in the in vitro allograft reaction than spleen cells from virgin mice. However, when spleen cells freshly harvested from allogeneically mated mice were tested in a direct 51Cr release assay, lysis of target cells bearing the paternal alloantigens was demonstrable in only one-third of the experiments. It is proposed that T cell immunisation to paternal alloantigens occurs in pregnancy, but that cell-mediated cytotoxicity is inhibited.

Animals↗
PubMed1979

[Immunological aspects of interactions between mother and foetus (author's transl)].

The essential information about materno-foetal immunologic interactions is reviewed. After a brief description of placental tissue (decidual cells from uterine mucosa, trophoblast), evidence that immunisation can be achieved by introduction of antigen into normal uterus is presented, although grafts performed in uterus of pregnant females are prolonged. Throphoblast cells bear specific antigens but histocompatibility antigens are usually not detectable at their surface. Proteins and cells from the foetus enter the maternal circulation and vice-versa, resulting in the production of antibodies against cell-associated foetal antigens by the mother. Some regulatory process of the maternal immune response have been investigated including blocking antibodies, maternal and foetal suppressor T cells. The biological roles of trophoblast and that of sustained microchimerism are underlined. Immunologic damage to the foetus can be produced only by inducing a cytotoxic cellular response before pregnancy. Possible analogies between immune responses to foetal allografts and tumors are discussed.

Allergy and Immunology↗
PubMed2026

Changes of DNA methylation and gene expression profile in placental villi and chorioamniotic membranes under preeclampsia.

BACKGROUND: Preeclampsia (PE) is a serious pregnancy complication with elusive pathogenesis. Although epigenetic dysregulation is implicated, its layer-specific placental roles are poorly defined. This study aimed to identify shared and layer-specific epigenetic alterations in PE by profiling DNA methylation and gene expression in placental villi (PV) and chorioamniotic membranes (CAM). RESEARCH DESIGN AND METHODS: PV and CAM samples were collected from 7 normal and 8 PE pregnancies, and three public DNA methylation datasets (GSE98224, GSE44667, GSE75196) were integrated. Differentially methylated genes (DMGs) and differentially expressed genes (DEGs) were identified based on whole-genome methylation and transcriptome sequencing. Layer-specific and shared gene sets were identified by cross-analysis, with functional annotation using Gene Ontology (GO). RESULTS: EM-seq revealed a hypermethylation-dominant, tissue-specific methylation landscape in PE placentas. Cross-tissue comparison identified shared DMGs between the two layers, including nine key genes consistently altered in public datasets. Integrated analysis in PV further identified 22 co-dysregulated genes, enriched in thermoregulation, maternal-fetal immunity, signal transduction, and cell differentiation. CONCLUSIONS: This study elucidates the shared and layer-specific dysregulation of gene networks at methylomic and transcriptomic levels in PE placenta. Comparing PV and CAM highlights placental epigenetic heterogeneity and dysfunction, offering novel clues for mechanistic research and layer-targeted therapies.

Humans↗
PubMed2026

MX1+ effector T cells hyperactivation at the maternal-fetal interface in unexplained recurrent pregnancy loss.

BACKGROUND: Immune tolerance breakdown at the maternal-fetal interface is implicated in unexplained recurrent pregnancy loss (URPL), but the interplay between T cell hyperactivation and dendritic cells (DCs)-mediated signaling remains poorly defined. METHODS: First-trimester decidual tissues from 5 healthy controls and 6 URPL patients underwent single-cell RNA sequencing (scRNA-seq, 10× Genomics). Computational analyses included clustering (Seurat), trajectory inference (scTour), intercellular communication (CellChat) and metabolic pathway enrichment (Gene Ontology and scMetabolism). Flow cytometry was performed from 11 patients and 11 healthy controls. Spatial validation was performed via multiplex immunohistochemistry and immunohistochemistry on 12 additional controls and 12 URPL cases. Statistical significance was assessed using Student’s t-test. RESULTS: URPL decidua exhibited marked CD3+ T cells and MX1+effector T (Tem) cells infiltration and activation. Flow cytometry analysis confirmed a significant decidua-specific upregulation of T cell activation markers CD25 and CD69 specifically on the MX1+Tem subset in URPL patients compared to controls. MX1+Tem cell subset demonstrated interferon hyperactivation, proliferative hyperactivity and lipid-biased immunometabolism. Pseudotemporal analysis positioned MX1+ Tem cells between classical Tem and exhausted T cell states, suggesting progressive differentiation. CellChat identified DCs as key regulators of MX1+ Tem expansion via aberrant ICOSL signaling, validated by spatial co-localization of ICOSL+ DCs and MX1+ Tem cells in URPL tissues. CONCLUSION: Our findings demonstrate that the aberrant activation and proliferation of MX1+Tem cells as a key immunological feature associated with URPL patients.

Humans↗
PubMed1976

Effect of antiserum on transplantable hematopoietic colony-forming units during Rauscher leukemia development.

Studies have been carried out to determine the sensitivity of hematopoietic CFU-S from Rauscher leukemic mice to an antiserum against the disease prepared in syngeneic mice. Test of this antiserum against Rauscher virus prior to injection showed it to be effective both in vitro and in vivo. At the same time, normal serum was shown to be without effect either against the CFU-S or against the virus. Spleen CFU-S were obtained from control and leukemic mice over a sequence of days following Rauscher virus injection and assayed by transplantation technique. Prior to transplantation these were incubated in vitro in either normal syngeneic serum or syngeneic antiserum. Incubation with antiserum had no effect on CFU-S obtained from the spleens of normal mice. However, incubation in this antiserum of spleen CFU-S from Rauscher leukemic mice resulted in a reduction of up to 50% in their colony-forming ability. Additional tests with guinea pig complement suggested that the levels of inactivation seen are not complement limited. This antiserum-induced reduction in colony formation was first evident in the second week after the injection of virus, coincident with the onset of splenomegaly in the leukemic mice. Thereafter, sensitivity of CFU-S to the antiserlm could be detected up to the terminal point of the leukemia (44 days).

Animals↗
PubMed2026

Epigenetic and immunological alterations in umbilical cord blood of overweight/obese women with gestational diabetes mellitus: insights into DNA methylation signatures and immune cell dysregulation.

BACKGROUND: Gestational diabetes mellitus (GDM) is a common pregnancy complication associated with adverse maternal and neonatal outcomes. Epigenetic modifications may reflect intrauterine metabolic exposure and contribute to immune and metabolic alterations. This study aimed to explore DNA methylation profiles in umbilical cord blood from overweight and obese women with and without GDM. METHODS: Umbilical cord blood samples from 30 overweight/obese pregnant women (with and without GDM) were analyzed using the Illumina 850&#xa0;K methylation array to identify differentially methylated positions (DMPs) and regions (DMRs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to assess the functional relevance of methylation changes. Immune cell composition was estimated using deconvolution analysis and further examined in an independent single-cell RNA sequencing (scRNA-seq) cohort. Lasso regression was applied to identify CpG sites associated with GDM status and construct a preliminary methylation-based classification model. RESULTS: A total of 23,331 hypermethylated and 29,501 hypomethylated DMPs were identified between women with and without GDM, with hypomethylation predominating. Enrichment analyses indicated associations with neurodevelopmental pathways, metabolic processes, immune regulation, and epigenetic modification. Immune deconvolution analysis suggested reduced proportions of CD4+ T cells (p&#x2009;<&#x2009;0.05) and a trend toward decreased NK cells in the GDM group, alongside increased CD8+ T cells and neutrophils. Seven CpG sites were selected for model construction and demonstrated strong discriminatory performance within this cohort. CONCLUSION: This exploratory study identifies distinct cord blood DNA methylation patterns associated with GDM in overweight/obese pregnancies. The findings suggest potential links between epigenetic alterations and immune cell composition in GDM-exposed offspring. The identified CpG signature warrants further validation in larger, prospective cohorts to determine its clinical applicability.

Humans↗
PubMedDate not supplied

The V gene repertoire as revealed by polyclonal B cell activators.

The evidence for the one non-specific signal hypothesis stating that the B lymphocytes are activated by non-clonally distributed receptors which are not the Ig receptors, have been summarized. Even though protein A is a polyclonal B cell activator, it does not exert its effect by interacting with the Fc part of Ig receptors. One consequence of the one non-specific signal concept is that thymus-dependent antigens cannot activate or tolerize B cells. It was shown that B cells from animals tolerant to a thymus-dependent protein antigen could be activated by polyclonal B cell activators to produce antibodies against the tolerogen. Experimentally induced tolerance did not differ from tolerance to self antigens, since LPS and PPD induced autoantibodies capable of lysing autologous red cells and isotope labelled autologous and syngeneic spleen cells. Thus, B cells cannot discriminate self from nonself whereas T cells have been shown to possess this ability.

Animals↗
PubMed1978

Placental coccidioidomycosis without fetal disease.

We encountered two cases of maternal coccidioidomycosis with placental involvement. Altered cell-mediated immunity during pregnancy makes the diagnosis of desseminated coccidioidomycosis difficult by the routine serologic tests; placental examination provides specific information. A high index of suspicion regarding this disease and prompt institution of appropriate therapy are necessary in order to decrease maternal and neonatal mortality.

Adult↗
PubMed1975

Presence of thymic antigen on rabbit basophils.

A goat heteroantiserum specific for a rabbit thymus lymphocyte antigen (RTLA) reacted with rabbit basophils resulting in the release of histamine. This activity was equally absorbed out by thymocytes or basophils. Absorption with either of these cell types also resulted in equal loss of thymocytotoxicity. No effect in either system occurred after absorption with either granulocytes or rabbit fibroblasts. These results could not be explained by the presence of immune complexes or aggregated globulin present in the RTLA antiserum. Further, the RTLA anti-serum had no anti-IgE activity, as demonstrated by its lack of reactivity with mast cells that were otherwise capable of releasing histamine normally after challenge with antigen. We have thus shown a basic difference between mast cells and basophils. We conclude that the rabbit basophil may bear a thymic marker.

Absorption↗
PubMed1978

Plasmodium berghei adoptive transfer and immunosuppression of immunity in allogenic neonates.

Outbred female rats were hyperimmunized with Plasmodium berghei and mated to produce progeny. Spleen cells from the immunized rats and from normal control mothers were adoptively transferred to their 48 hr old neonates. Some neonates from immune mothers were fostered to normal mothers and vice versa. Weanling rats were challenged 35 days after birth with Plasmodium berghei; immune and normal litters which had not received cells were also challenged at the same time. Rats which had received immune spleen cells from their mothers but were fostered on to non-immune mothers showed significantly lower parasitaemias and higher fluorescent antibody titres than any other combination of cell transfer and maternal milk. GVH reaction was minimal. These results suggest that the immune response to P. berghei was suppressed in the presence of passively transferred maternal antibody.

Animals↗