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Cationic Magnetic Nanoparticles Activate Natural Killer Cells for the Treatment of Glioblastoma.
ACS Nano
January 2025
Key Laboratory of Biomedical Polymers of Ministry of Education and Department of Chemistry, Wuhan University, Wuhan 430072, P. R. China.
The blood-brain barrier (BBB) and the immunosuppressive microenvironment of glioblastoma (GBM) severely hinder the infiltration and activity of natural killer (NK) cells, thereby reducing their clinical efficacy in GBM treatment. To address this challenge, we introduced an engineered living material, HEFDS-NK cells, designed to enhance the penetration of NK cells across the BBB and improve their cytotoxicity against GBM. HEFDS comprises magnetic nanoparticles modified using cationic polyethylenimine (PEI), selenocysteine (Sec), and sodium hyaluronate (HA) and cocultured with NK cells to form HEFDS-NK cells.
View Article and Find Full Text PDFTocilizumab and immune signatures for targeted management of cytokine release syndrome in immune checkpoint therapy.
Ann Oncol
December 2024
Centre Hospitalier Universitaire Vaudois (CHUV), University of Lausanne, Department of Medicine, Immunology and Allergy Service, Rue du Bugnon 46, CH-1011 Lausanne, Switzerland. Electronic address:
Article Synopsis
- The study identifies biomarkers that can differentiate between immune-related cytokine release syndrome (irCRS) and sepsis in oncology patients undergoing immune checkpoint inhibitor therapy.
- The analysis revealed that hepatocyte growth factor (HGF) and ferritin are particularly effective in predicting outcomes related to irHLH and Grade 3 irCRS, with a 100% positive and negative predictive value.
- Patients with severe irCRS who did not respond to corticosteroids showed complete resolution after treatment with tocilizumab (TCZ), highlighting the potential for targeted therapies in these cases.
The effector PieF modulates mRNA stability through association with eukaryotic CCR4-NOT.
mSphere
December 2024
Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.
Unlabelled: The eukaryotic CCR4-NOT deadenylase complex is a highly conserved regulator of mRNA metabolism that influences the expression of the complete transcriptome, representing a prime target for a generalist bacterial pathogen. We show that a translocated bacterial effector protein, PieF (Lpg1972) of , directly interacts with the CNOT7/8 nuclease module of CCR4-NOT, with a dissociation constant in the low nanomolar range. PieF is a robust inhibitor of the DEDD-type nuclease, CNOT7, acting in a stoichiometric, dose-dependent manner.
View Article and Find Full Text PDFTOE1 deadenylase inhibits gastric cancer cell proliferation by regulating cell cycle progression.
Biochim Biophys Acta Gen Subj
January 2025
Beijing International Science and Technology Cooperation Base of Antivirus Drug, College of Chemistry and Life Science, Beijing University of Technology, Beijing 100124, China. Electronic address:
TOE1, also known as hCaf1z, belongs to the DEDD superfamily of deadenylases and a newly identified isoenzyme of hCaf1 deadenylases. Previous research has demonstrated that TOE1 has deadenylase activity, which can catalyze the degradation of poly(A) substrates and interact with hCcr4d to form the unconventional human Ccr4-Caf1 deadenylase complex. Our recent research indicates that hCaf1a and hCaf1b isoenzymes, highly expressed in gastric cancer, promote gastric cancer cell proliferation and tumorigenicity via modulating cell cycle progression.
View Article and Find Full Text PDFThe FGFR inhibitor Rogaratinib reduces microglia reactivity and synaptic loss in TBI.
Front Immunol
December 2024
Department of Neurology, Ulm University, Ulm, Germany.
Background: Traumatic brain injury (TBI) induces an acute reactive state of microglia, which contribute to secondary injury processes through phagocytic activity and release of cytokines. Several receptor tyrosine kinases (RTK) are activated in microglia upon TBI, and their blockade may reduce the acute inflammation and decrease the secondary loss of neurons; thus, RTKs are potential therapeutic targets. We have previously demonstrated that several members of the Fibroblast Growth Factor Receptor (FGFR) family are transiently phosporylated upon TBI; the availability for drug repurposing of FGFR inhibitors makes worthwhile the elucidation of the role of FGFR in the acute phases of the response to TBI and the effect of FGFR inhibition.
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