ArticleInternational journal of inflammation2010
The regulation of the CNS innate immune response is vital for the restoration of tissue homeostasis (repair) after acute brain injury: a brief review.
Article in International journal of inflammation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 55 citations in OpenAlex.
- Tandem mass tag-based serum proteomic profiling revealed diabetic foot ulcer pathogenesis and potential therapeutic targets.Bioengineered · 2022Trial
- Multifaceted Immune Effects of the Scavenger Receptor CD36 on Long-Term Outcomes After Neonatal Arterial Focal Stroke.Journal of neurochemistry · 2026Article
- Spatiotemporal profile of an optimal host response to virus infection in the primate central nervous system.PLoS pathogens · 2025Article
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- ELEVATED SERUM C-REACTIVE PROTEIN LEVELS IN COVID-19 PATIENTS WITH SCIATICA: IMPLICATIONS FOR PROGNOSIS AND TREATMENT STRATEGIES.Acta clinica Croatica · 2024Article
- Intertwined pathways of complement activation command the pathogenesis of lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022Review
- First study on response of astrocytes in alevines of red-bellied pacu (Veterinary world · 2022Article
- Article
- NLRP1 Inflammasomes: A Potential Target for the Treatment of Several Types of Brain Injury.Frontiers in immunology · 2022Review
- Critical Roles of Lysophospholipid Receptors in Activation of Neuroglia and Their Neuroinflammatory Responses.International journal of molecular sciences · 2021Review
- CD47 in the Brain and Neurodegeneration: An Update on the Role in Neuroinflammatory Pathways.Molecules (Basel, Switzerland) · 2021Review
- Neuroinflammatory responses in Parkinson's disease: relevance of Ibuprofen in therapeutics.Inflammopharmacology · 2021Review
- COVID-Pain: Acute and Late-Onset Painful Clinical Manifestations in COVID-19 - Molecular Mechanisms and Research Perspectives.Journal of pain research · 2021Review
- The Role of Neuronal NLRP1 Inflammasome in Alzheimer's Disease: Bringing Neurons into the Neuroinflammation Game.Molecular neurobiology · 2019Review
- Complement and coagulation cascades in trauma.Acute medicine & surgery · 2019Review
- The Neuro-Immune-Regulators (NIREGs) Promote Tissue Resilience; a Vital Component of the Host's Defense Strategy against Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018Review
- Piperlongumine Improves Lipopolysaccharide-Induced Amyloidogenesis by Suppressing NF-KappaB Pathway.Neuromolecular medicine · 2018Article
- Ionizing Radiation-Induced Immune and Inflammatory Reactions in the Brain.Frontiers in immunology · 2017Review
- Functional connectivity structure of cortical calcium dynamics in anesthetized and awake mice.PloS one · 2017Article
- CD200 restrains macrophage attack on oligodendrocyte precursors via toll-like receptor 4 downregulation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurons and glia respond to acute injury by participating in the CNS innate immune response. This involves the recognition and clearance of "not self " pathogens and "altered self " apoptotic cells. Phagocytic receptors (CD14, CD36, TLR-4) clear "not self" pathogens; neurons and glia express "death signals" to initiate apoptosis in T cells.The complement opsonins C1q, C3, and iC3b facilitate the clearance of apoptotic cells by interacting with CR3 and CR4 receptors. Apoptotic cells are also cleared by the scavenger receptors CD14, Prs-R, TREM expressed by glia. Serpins also expressed by glia counter the neurotoxic effects of thrombin and other systemic proteins that gain entry to the CNS following injury. Complement pathway and T cell activation are both regulated by complement regulatory proteins expressed by glia and neurons. CD200 and CD47 are NIRegs expressed by neurons as "don't eat me" signals and they inhibit microglial activity preventing host cell attack. Neural stem cells regulate T cell activation, increase the Treg population, and suppress proinflammatory cytokine expression. Stem cells also interact with the chemoattractants C3a, C5a, SDF-1, and thrombin to promote stem cell migration into damaged tissue to support tissue homeostasis.
Identifiers
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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.