Description
OEP005161
Description
OEP004403
Description
OEP003180
DescriptionIn the course of immune development, HIV-exposed uninfected (HEU) infants exhibit abnormal immune function and higher infectious morbidity compared to HIV-unexposed uninfected (HUU) infants. Yet functional phenotypes and the regulators associated with in-utero HIV exposure remain largely obscure. Herein, we utilized flow cytometry and RNA-seq technologies to establish the immune and transcriptional profiling in cord blood from 9 HEU mother-infant pairs and 24 HUU pairs. On top of that, we compared the cord blood dataset with the maternal venous blood dataset to characterize the unique effects induced by in-utero HIV exposure. Flow cytometry immunophenotyping revealed a significant decrease in the level of B lymphocyte subsets in HEU cord blood compared to HUU cord blood. Expression profiling-based assessment of cell abundance indicated a marked reduction in naive B cells in HEU cord blood, supporting the altered composition of B lymphocyte subsets in HEU infants. Functional enrichment results demonstrated a propensity for suppressed innate immune responses and impaired immune regulatory function of B cells in HEU cord blood. Additionally, through a combination of differential expression analysis, co-expression network analysis, and feature selection analysis, we identified an immunologically significant HEU-related signature. This 4-gene signature could effectively assess B cell levels in cord blood, enabling discrimination between HEU and HUU infants. This study provides the first transcriptomic characterization of HEU cord blood compared to maternal venous blood and establishes a 4-gene-based classifier for predicting immunological abnormalities in HEU infants. These findings hold promise for uncovering new mechanisms underlying abnormal immune system development in infants due to in-utero HIV exposure.
OEP005165
DescriptionAlteration of cell metabolism is one of the essential characteristics of tumor growth. Cancer stem cells (CSCs) are the initiating cells of tumorigenesis, proliferation, recurrence, and other processes, and play an important role in therapeutic resistance and metastasis. Thus, identification of the metabolic profiles in prostate cancer stem cells (PCSCs) is critical to understanding prostate cancer progression. Here, using untargeted metabolomics and lipidomics methods, we showed distinct metabolic differences between prostate cancer cells and PCSCs. We obtained DU145 spheres by ultralow-attached culture in sphere conditional medium. We use serum-induced sphere (adherent state) as control (Adh), and generation 2 (G2) and generation 3 (G3) of spheres as experimental groups to study the metabolic changes between prostate cancer cells and cancer stem cells.
OEP004085
DescriptionRNA-seq of photorespiratory bypass plants
Used IDNODEP00000033  
OEP000073
DescriptionRNA-seq and MeRIP-seq data
OEP004978
DescriptionCarotid endarterectomy (CEA) has been widely employed to treat Carotid artery stenosis (CAS). Yet, the impact of CEA on CAS-induced cognitive impairment and underlying mechanisms remain poorly understood.
OEP005154
DescriptionCancer associated fibroblasts (CAFs) have been shown to play a crucial role in regulating tumor chemotherapy and immunotherapy resistance. The therapeutic value of CAFs in prostate cancer has largely not been studied. Our research revealed that CAFs secrete CCL5, which promotes the upregulation of androgen receptor (AR) expression in prostate cancer cells, leading to resistance to enzalutamide therapy. Furthermore, CCL5 also enhances the expression of tumor programmed death-ligand 1 (PD-L1), resulting in immune escape. Mechanistically, CCL5 binds to its receptor, CC motif chemokine receptor 5 (CCR5), on prostate cancer cells and activates the AKT signaling pathway, leading to the upregulation of AR and PD-L1. The CCR5 antagonist maraviroc to inhibit the CAFs mediated CCL5 signaling pathway can effectively reduce the expression of AR and PD-L1, and improve the efficacy of enzalutamide. Together, CAFs can enhance the expression of AR and PD-L1 by paracrine CCL5 binding to CCR5 activated AKT pathway in prostate cancer, resulting in enzalutamide resistance and immune escape. And targeting CCL5-CCR5 communication as a promising treatment method to improve the effectiveness of enzalutamide.
OEP005133
Description
OEP005148