Ontology highlight
ABSTRACT:
PROVIDER: PRJNA755822 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15507400_1.fastq.gz | Fastqsanger.gz | |||
| SRR15507400_2.fastq.gz | Fastqsanger.gz | |||
| SRR15507401_1.fastq.gz | Fastqsanger.gz | |||
| SRR15507401_2.fastq.gz | Fastqsanger.gz | |||
| SRR15507402_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 192 |
Similar Datasets
Project description:During pregnancy, immune responses must balance fetal protection from infections with tolerance of the semi-allogeneic fetus. However, the mechanisms regulating maternal-fetal tolerance remain poorly understood. Recently, we identified KIR+CD8+ T cells as a previously underappreciated regulatory subset important for suppressing self-reactivity in human autoimmune and infectious diseases. To better understand what other roles these cells might play, we asked whether they are active during pregnancy. We first observed an increased frequency of KIR+CD8+ T cells in the peripheral blood of pregnant women at the second trimester, especially in those carrying a male fetus. In vitro, KIR+CD8+ T cells inhibited the alloreactive responses of maternal T cells against irradiated cord blood cells and suppressed HY-specific CD8+ T cells from mothers with a male fetus. Therefore, the higher induction of KIR+CD8+ T cells in mothers carrying a male fetus may help suppress additional allogenic responses triggered by Y chromosome antigens. Longitudinal analysis showed that KIR+CD8+ T cells undergo expansion and differentiate into functional cytotoxic cells during pregnancy. Single cell RNA-seq analysis of decidual CD8+ T cells from early pregnancy revealed elevated number and activity of KIR+ CD8+ T cells at the maternal-fetal interface. In addition, increased levels of KIR+CD8+ T cells correlated with pregnancy disorders (e.g., spontaneous abortion and preeclampsia). Taken together, our findings suggest an important role of KIR+CD8+ T cells in the maintenance of maternal tolerance by suppressing fetal-specific alloreactive T cells. They may also be useful as predictive biomarkers or drug targets for human pregnancy disorders.
2025-08-01 | GSE281341 | GEO
Project description:Immunological tolerance during pregnancy is necessary for women’s bodies to accept the semi-allogenic fetus. Interestingly, “immune evasion”, which consists of some similar immunological changes, was recently proposed as a hallmark of cancer. Looking at these results, it seems paradoxical that increasing number of full-term pregnancies (FTP) reduces the risk of breast cancer in women. Our aim was to use a systems epidemiology approach to investigate this paradox by modelling breast cancer incidence as a function of parity in the Norwegian Women and Cancer (NOWAC) cohort, then testing the mathematical model using gene expression from blood in a subcohort of these women: the NOWAC postgenome cohort. Lastly, we undertook a gene set enrichment analysis for immunological gene sets. A linear trend nicely fitted the dataset showing an 8% decrease in risk for each FTP, independent of stratification on other risk factors and lasting for decades after a woman’s last FTP. However, when we looked at gene expression we found that hundreds of genes showed linear trends in cancer-free controls, but this was not the case in /any/ of the samples from breast cancer cases. In the gene set enrichment analysis, samples consisted of human blood or cord blood and mouse bone marrow or spleen. We found more adaptive gene sets than expected in humans and more innate gene sets than expected in mice. None of the gene sets provided information about the long-term effects of immunological tolerance during pregnancy, but the lack of relevant reductionist experiments hampers our interpretation. We suggest that, after resolution at birth, the immunological tolerance induced by pregnancy augments immune response to cancer development.
| EGAS00001002616 | EGA
Project description:There is increasing concern regarding the adverse effects of air pollution on human health, and benzene is a major toxic compound in air pollution. Maternal benzene exposure has been associated with reproductive complications, such as preterm birth, low birth weight, and immunological and neurological complications in the offspring. However, it is poorly understood how benzene induces these complications. Our objective was to establish a full body inhalation mouse model for maternal benzene exposure that mimics clinical phenotypes observed in human populations, and characterize the maternal immune activation and placental response in our model. Here, we report that maternal immune activation triggered by benzene exposure during pregnancy leads to increased resorptions, abnormal placenta development and low birth weight of fetus. More importantly, there is a sexual dimorphic response to benzene exposure in female and male placentas. In the male placenta, the transcriptome changes reveal a more immunologically relevant profile, while females have a metabolically related profile. Furthermore, we discover the sexual dimorphic response could be a consequence of the sexual dimorphism of placenta at baseline, which indicates the significant difference between sexes in terms of the immunological processes in the placenta, both in human and mouse. Therefore, our findings established a benzene exposure mouse model and indicated the sexual dimorphism of placenta, which provides valuable reference for the future pregnancy studies.
2023-07-20 | PXD035085 | Pride
Project description:mTEC/Tcell crosstalk drives epigenetic programs conditioning immunological tolerance
2022-01-24 | GSE144680 | GEO
Project description:ATAC-seq analysis of CD8 T cells after pregnancy-induced tolerance/hypofunction. The goal of this experiment was to compare the epigenetic effect of pregnancy on naive vs. memory fetus-specific CD8 T cells. We also included naive and skin-sensitized CD8 T cells (without pregnancy) as controls.
2023-05-03 | GSE216105 | GEO
Project description:Group 2 innate lymphoid cells (ILC2) promote the production of a type-2 immunological environment in the uterus and have tissue-specific gene signatures that change with pregnancy.
2023-04-15 | E-MTAB-5803 | biostudies-arrayexpress
Project description:Group 2 innate lymphoid cells (ILC2) promote the production of a type-2 immunological environment in the uterus and have tissue-specific gene signatures that change with pregnancy.
2023-04-15 | E-MTAB-5806 | biostudies-arrayexpress
Project description:There is a close relationship between pregnancy and immune responses. For example, an anti-inflammatory state is essential for maintaining pregnancy by promoting maternal tolerance toward the semi-allogeneic fetus, whereas pro-inflammatory conditions are crucial for processes such as maternal tissue remodeling during embryo implantation and the induction of labor. Increasing evidence suggests that various cell types within the uteroplacental immune environment contribute to these immune responses, and immunological approaches have been employed to investigate the pathophysiology and potential treatments of pregnancy-related complications. Interleukin-18 (IL-18) is a unique cytokine with both pro-inflammatory and anti-inflammatory properties; however, its roles during pregnancy remain largely unclear. We have found that smooth muscle cells (SMCs) in the uterine myometrium are an important source of IL-18, and that the homeostatic production of IL-18 promotes fetal development by supporting maternal uterine remodeling and placental growth. To further investigate the effects of IL-18 on the uterine immune milieu, we established SMC-specific Il18 conditional knockout (cKO) mice and performed RNA sequencing of uterine immune cells.
2025-04-18 | GSE293908 | GEO
Project description:Maintenance of immunological homeostasis between tolerance and autoimmunity is essential for the prevention of human diseases ranging from autoimmune disease to cancer. Accumulating evidence suggests that p53 can mitigate phagocytosis-induced adjuvanticity thereby promoting immunological tolerance following programmed cell death. Here we identify Inhibitor of Apoptosis Stimulating p53 Protein (iASPP), a negative regulator of p53 transcriptional activity, as a regulator of immunological tolerance. iASPP-deficiency promoted lung adenocarcinoma and pancreatic cancer tumorigenesis, while iASPP-deficient mice were less susceptible to autoimmune disease. Immune responses to iASPP-deficient tumors exhibited hallmarks of immunosuppression, including activated regulatory T cells and exhausted CD8+ T cells. Interestingly, iASPP-deficient tumor cells and tumor-infiltrating myeloid cells, CD4+, and γδ T cells expressed elevated levels of PD-1H, a recently identified transcriptional target of p53 that promotes tolerogenic phagocytosis. Identification of an iASPP/p53 axis of immune homeostasis provides a therapeutic opportunity for both autoimmune disease and cancer.
2023-02-02 | GSE202445 | GEO
Project description:Maintenance of immunological homeostasis between tolerance and autoimmunity is essential for the prevention of human diseases ranging from autoimmune disease to cancer. Accumulating evidence suggests that p53 can mitigate phagocytosis-induced adjuvanticity thereby promoting immunological tolerance following programmed cell death. Here we identify Inhibitor of Apoptosis Stimulating p53 Protein (iASPP), a negative regulator of p53 transcriptional activity, as a regulator of immunological tolerance. iASPP-deficiency promoted lung adenocarcinoma and pancreatic cancer tumorigenesis, while iASPP-deficient mice were less susceptible to autoimmune disease. Immune responses to iASPP-deficient tumors exhibited hallmarks of immunosuppression, including activated regulatory T cells and exhausted CD8+ T cells. Interestingly, iASPP-deficient tumor cells and tumor-infiltrating myeloid cells, CD4+, and gamma-delta T cells expressed elevated levels of PD-1H, a recently identified transcriptional target of p53 that promotes tolerogenic phagocytosis. Identification of an iASPP/p53 axis of immune homeostasis provides a therapeutic opportunity for both autoimmune disease and cancer.
2023-02-02 | GSE202443 | GEO