ArticleThe American journal of pathology2000
Spontaneous classical pathway activation and deficiency of membrane regulators render human neurons susceptible to complement lysis.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 134 citations in OpenAlex.
- Involvement of Complement in Alzheimer's Disease: From Genetics Through Pathology to Therapeutic Strategies.Current topics in behavioral neurosciences · 2025Review
- The complement system in neurodegenerative diseases.Clinical science (London, England : 1979) · 2024Article
- The Role of Complement Dysregulation in Glaucoma.International journal of molecular sciences · 2024Review
- Article
- Microglia-neuron interactions in prefrontal gray matter in schizophrenia: a postmortem ultrastructural morphometric study.European archives of psychiatry and clinical neuroscience · 2023Article
- Targeting the complement system in neuromyelitis optica spectrum disorder.Expert opinion on biological therapy · 2021Review
- Modulation of the Complement System by Neoplastic Disease of the Central Nervous System.Frontiers in immunology · 2021Review
- Complement C6 deficiency exacerbates pathophysiology after spinal cord injury.Scientific reports · 2020Article
- The effect of insomnia on development of Alzheimer's disease.Journal of neuroinflammation · 2020Review
- C1q Regulates Horizontal Cell Neurite Confinement in the Outer Retina.Frontiers in neural circuits · 2020Article
- Complement-dependent bystander injury to neurons in AQP4-IgG seropositive neuromyelitis optica.Journal of neuroinflammation · 2018Article
- 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
- Complement Component C3 Promotes Cerebral Ischemia/Reperfusion Injury Mediated by TLR2/NFκB Activation in Diabetic Mice.Neurochemical research · 2018Article
- Complement in the pathogenesis of Alzheimer's disease.Seminars in immunopathology · 2018Review
- Comprehensive review of neuromyelitis optica and clinical characteristics of neuromyelitis optica patients in Puerto Rico.Surgical neurology international · 2018Review
- ChronicJournal of oral microbiology · 2017Article
- Long-Term Estrogen Receptor Beta Agonist Treatment Modifies the Hippocampal Transcriptome in Middle-Aged Ovariectomized Rats.Frontiers in cellular neuroscience · 2016Article
- Porphyromonas gingivalis Periodontal Infection and Its Putative Links with Alzheimer's Disease.Mediators of inflammation · 2015Review
- Article
- Longitudinally extensive NMO spinal cord pathology produced by passive transfer of NMO-IgG in mice lacking complement inhibitor CD59.Journal of autoimmunity · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
Abstract
This study investigated the capacity of neurons and astrocytes to spontaneously activate the complement system and control activation by expressing complement regulators. Human fetal neurons spontaneously activated complement through the classical pathway in normal and immunoglobulin-deficient serum and C1q binding was noted on neurons but not on astrocytes. A strong staining for C4, C3b, iC3b neoepitope and C9 neoepitope was also found on neurons. More than 40% of human fetal neurons were lysed when exposed to normal human serum in the presence of a CD59-blocking antibody, whereas astrocytes were unaffected. Significant reduction in neuronal cell lysis was observed after the addition of soluble complement receptor 1 at 10 microg/ml. Fetal neurons were stained for CD59 and CD46 and were negative for CD55 and CD35. In contrast, fetal astrocytes were strongly stained for CD59, CD46, CD55, and were negative for CD35. This study demonstrates that human fetal neurons activate spontaneously the classical pathway of complement in an antibody-independent manner to assemble the cytolytic membrane attack complex on their membranes, whereas astrocytes are unaffected. One reason for the susceptibility of neurons to complement-mediated damage in vivo may reside in their poor capacity to control complement activation.
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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.