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| http://dx.doi.org/10.18632/oncotarget.5249 | DOI Listing |
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IL-33-activated ILC2s induce tertiary lymphoid structures in pancreatic cancer.
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Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Tertiary lymphoid structures (TLSs) are de novo ectopic lymphoid aggregates that regulate immunity in chronically inflamed tissues, including tumours. Although TLSs form due to inflammation-triggered activation of the lymphotoxin (LT)-LTβ receptor (LTβR) pathway, the inflammatory signals and cells that induce TLSs remain incompletely identified. Here we show that interleukin-33 (IL-33), the alarmin released by inflamed tissues, induces TLSs.
View Article and Find Full Text PDFCorrigendum to "The role of α7nAchR and PD-L1 in neuroimmune regulation of keloid treatment" [Cellular Signalling, Volume 121 (2024), Article 111275].
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LncRNA NEAT1, an Important Biomarker Involved in the Pathological and Physiological Processes of Parkinson's Disease.
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Department of Cardiothoracic Surgery, Children's Hospital of Nanjing Medical University, Nanjing, 210008, China.
Parkinson's disease (PD) is a complex progressive neurodegenerative disorder and the pathogenesis and treatment methods are unknown. This aim is to investigate the effects of long non coding RNA NEAT1 (LncRNA NEAT1) on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease (PD). Immunoprecipitation and western blot were used to search for the effects of LncRNA NEAT1 on PD.
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January 2025
2Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia, USA; email:
Regulation of the brain's neuroimmune system is central to development, normal function, and disease. Neuronal communication to microglia, the primary immune cells of the brain, is well known to involve purinergic signaling mediated via ATP secretion and the cytokine fractalkine. Recent evidence shows that neurons release multiple cytokines beyond fractalkine, yet these are less studied and poorly understood.
View Article and Find Full Text PDFFrom Homeostasis to Neuroinflammation: Insights into Cellular and Molecular Interactions and Network Dynamics.
Cells
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Max Planck Institute for Human Development, Lentzeallee 94, 14195 Berlin, Germany.
Neuroinflammation is a complex and multifaceted process that involves dynamic interactions among various cellular and molecular components. This sophisticated interplay supports both environmental adaptability and system resilience in the central nervous system (CNS) but may be disrupted during neuroinflammation. In this article, we first characterize the key players in neuroimmune interactions, including microglia, astrocytes, neurons, immune cells, and essential signaling molecules such as cytokines, neurotransmitters, extracellular matrix (ECM) components, and neurotrophic factors.
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