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Targeting immune checkpoints on myeloid cells: current status and future directions.
Cancer Immunol Immunother
January 2025
Department of General Surgery, Shengjing Hospital of China Medical University, ShenyangLiaoning Province, 110004, China.
Myeloid cells accumulate extensively in most tumors and play a critical role in immunosuppression of the tumor microenvironment (TME). Like T cells, myeloid cells also express immune checkpoint molecules, which induce the immunosuppressive phenotype of these cells. In this review, we summarize the tumor-promoting function and immune checkpoint expression of four types of myeloid cells: macrophages, neutrophils, dendritic cells, and myeloid-derived suppressor cells, which are the main components of the TME.
View Article and Find Full Text PDFUpregulation of OGT-mediated EZH2 O-GlcNAcylation Promotes Human Umbilical Vein Endothelial Cell Proliferation, Invasion, Migration, and Tube Formation in Gestational Diabetes Mellitus.
Cell Biochem Biophys
January 2025
Department of Obstetrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, 361003, China.
O-linked N-acetylglucosamine transferase (OGT)-catalyzed O-linked N-acetylglucosamine glycosylation (O-GlcNAcylation) is closely associated with diabetes progression. This study aims to investigate the mechanism of OGT in regulating endothelial dysfunction in gestational diabetes mellitus (GDM). Expressions of OGT, O-linked N-acetylglucosamine (O-GlcNAc), enhancer of zeste homolog 2 (EZH2), and HEK27me3 in human umbilical vein endothelial cells (HUVECs) and GDM-derived HUVECs (GDM-HUVECs) were assessed by western blot.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Boston Children's Hospital, Boston, MA, USA.
Background: Alzheimer's disease (AD), an age-associated neurodegenerative disorder, is characterized by progressive neuronal loss and the accumulation of misfolded proteins such as amyloid-β and tau. While neuroinflammation, mediated by microglia and brain-resident macrophages, plays a pivotal role in AD pathogenesis, the intricate interactions among age, genes, and other risk factors remain elusive. Somatic mutations, known to accumulate with age, instigate clonal expansion across diverse cell types, impacting both cancer and non-cancerous conditions.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX, USA.
Background: In Alzheimer's disease (AD), changes in the brain transcriptome are hypothesized to mediate the impact of neuropathology on cognition. Gene expression profiling from postmortem brain tissue is a promising approach to identify causal pathways; however, there are challenges to definitively resolve the upstream pathologic triggers along with the downstream consequences for AD clinical manifestations.
Method: We have functionally dissected 30 AD-associated gene coexpression modules using a cross-species strategy in Drosophila melanogaster models.
Influence of stromal neural crest progenitor cells on neuroblastoma radioresistance.
Int J Radiat Biol
January 2025
Departamento de Biología Celular, Universidad de Sevilla, Seville, Spain.
Purpose: A substantial proportion of children with high risk Neuroblastoma die within the first 5 years post-diagnosis despite the complex treatment applied. In the recent years, tumor environment has been revealed as key factor for cancer treatment efficacy. In this sense, non-tumorigenic Neural Crest progenitor cells from high risk patients, have been described as part of Neuroblastoma stroma, promoting tumor growth and contributing to mesenchyme formation.
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