ReviewInternational journal of molecular sciences2024
Impact of TNF and IL-33 Cytokines on Mast Cells in Neuroinflammation.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 24 citations in OpenAlex.
- Xuebijing alleviates septic myocardial injury by inhibiting ferroptosis mediated by the ICAM1/TLR signaling pathway.Histology and histopathology · 2026Article
- The IL-33/ST2 pathway to modulate the inflammatory microenvironment: A new therapeutic target in chronic obstructive pulmonary disease.Biochemistry and biophysics reports · 2026Review
- Astrocyte-Microglia Crosstalk in Post-Hemorrhagic Neurovascular Microenvironment: Mechanistic Nodes, Cross-Stroke Comparisons, and Therapeutic Reprogramming.Translational stroke research · 2026Review
- Reframing ME/CFS: toward a unified mechanistic model of chronic post-infectious diseases.Journal of translational medicine · 2026Review
- Network Pharmacology Reveals the Therapeutic Potential of BBB-Permeable Compounds fromInternational journal of molecular sciences · 2026Article
- Review
- Developmental PBDE exposure persistently impairs mast cell function in vivo and drives sex-specific morphological and transcriptional changes in bone marrow-derived mast cells.Environmental research · 2026Article
- The Role of Mast Cells and Their Potential as a Therapeutic Target For Neuroinflammation.Journal of inflammation research · 2026Review
- Chronic Neuroplasticity Changes Following Neurotropic Viral Infection: Mechanisms and Implications.Cellular and molecular neurobiology · 2025Review
- An intermediate activation state primes Langerhans cell migration from the epidermis.bioRxiv : the preprint server for biology · 2025Article
- Bidirectional Interplay Between Microglia and Mast Cells.International journal of molecular sciences · 2025Review
- Aberrant Activation of Mast Cells: Molecular Mechanisms and Targets for Intervention.Clinical reviews in allergy & immunology · 2025Review
- Multi-omic biomarkers associated with multiple sclerosis: from Mendelian randomization to drug prediction.Scientific reports · 2025Article
- Article
- Protective role of savory essential oil on vital organs in rats against deleterious effects induced by lead acetate.Biotechnology reports (Amsterdam, Netherlands) · 2025Article
- Expression of Neuronal Nicotinic Acetylcholine Receptor and Early Oxidative DNA Damage in Aging Rat Brain-The Effects of Memantine.International journal of molecular sciences · 2025Article
- Identification and experimental validation of BMX as a crucial PANoptosis‑related gene for immune response in Spinal Cord Injury.PloS one · 2025Article
- Mechanisms of prostatic inflammation-mediated male lower urinary tract symptoms.American journal of clinical and experimental urology · 2025Review
- α7-Nicotinic Acetylcholine Receptor Activation Modulates BV2 Microglial Plasticity via miR-21/TNF-α/NFκB in Oxygen-Glucose Deprivation/Reoxygenation.Journal of molecular neuroscience : MN · 2024Article
- Histaminergic System Activity in the Central Nervous System: The Role in Neurodevelopmental and Neurodegenerative Disorders.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mast cells (MCs) are derived from hematopoietic progenitors, mature in vascularized tissues, and participate in innate and acquired immunity. Neuroinflammation is a highly debated topic in the biomedical literature; however, the impact of tumor necrosis factor (TNF) and IL-33 on MCs in the brain has not been widely addressed. MCs can be activated by IgE binding to FcεRI, as well as by different antigens. After activation, MCs mediate various immunological and inflammatory responses through TNF and IL-33. TNF has two receptors: TNFR1, a p55 molecule, and TNFR2, a p75 molecule. This cytokine is the only one of its kind to be stored in the granules of MCs and can also be generated by de novo synthesis via mRNA. In the central nervous system (CNS), TNF is produced almost exclusively by microglial cells, neurons, astrocytes, and, minimally, by endothelial cells. After its release into brain tissue, TNF rapidly induces the adhesion molecules endothelial leukocyte adhesion molecule 1 (ELAM-1), intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) in endothelial cells. TNF causes the chemoattraction of neutrophils by inducing several molecules, including CXC chemokines (IL-8). Both MCs and microglial cells act as a primary barrier against foreign molecules in the CNS, producing pro-inflammatory cytokines such as IL-33. IL-33 belongs to the IL-1 family, is activated through the ST2L/IL1-RAcP receptor complex, and mediates both the innate and adaptive immune response. IL-33 is a nuclear transcription factor expressed in the brain, where it induces pro-inflammatory cytokines (TNF and IL-1) and chemokines (CCL2, CCL3, CCL5, and CXCL10). Therefore, MCs and microglia in the CNS are a source of pro-inflammatory cytokines, including TNF and IL-33, that mediate many brain diseases. The inhibition of TNF and IL-33 may represent a new therapeutic approach that could complement existing neuroinflammatory therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.