ArticleActa neuropathologica2012
Intracerebral immune complex formation induces inflammation in the brain that depends on Fc receptor interaction.
Article in Acta neuropathologica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Article
- Adaptive immunity in the neuroinflammation of Alzheimer's disease.Chinese medical journal · 2025Review
- MS4A6A/Ms4a6d deficiency disrupts neuroprotective microglia functions and promotes inflammation in Alzheimer's disease model.Molecular neurodegeneration · 2025Article
- Neuroinflammation in Age-Related Neurodegenerative Diseases: Role of Mitochondrial Oxidative Stress.Antioxidants (Basel, Switzerland) · 2024Review
- Fenebrutinib, a Bruton's tyrosine kinase inhibitor, blocks distinct human microglial signaling pathways.Journal of neuroinflammation · 2024Article
- Article
- Amyloid Precursor Protein: A Regulatory Hub in Alzheimer's Disease.Aging and disease · 2024Review
- Serum immunoglobulin and the threshold of Fc receptor-mediated immune activation.Biochimica et biophysica acta. General subjects · 2023Review
- Bruton's tyrosine kinase inhibition reduces disease severity in a model of secondary progressive autoimmune demyelination.Acta neuropathologica communications · 2023Article
- Inflammaging and Frailty in Immune-Mediated Rheumatic Diseases: How to Address and Score the Issue.Clinical reviews in allergy & immunology · 2023Review
- Myelinating Co-Culture as a Model to Study Anti-NMDAR Neurotoxicity.International journal of molecular sciences · 2022Article
- Altered abundances of human immunoglobulin M and immunoglobulin G subclasses in Alzheimer's disease frontal cortex.Scientific reports · 2022Article
- Cognitive Decline in Rheumatoid Arthritis: Insight into the Molecular Pathogenetic Mechanisms.International journal of molecular sciences · 2021Review
- The Immunopathogenesis of Neuroinvasive Lesions of SARS-CoV-2 Infection in COVID-19 Patients.Frontiers in neurology · 2021Review
- The Functional Roles and Applications of Immunoglobulins in Neurodegenerative Disease.International journal of molecular sciences · 2020Review
- Dysregulated Fc gamma receptor-mediated phagocytosis pathway in Alzheimer's disease: network-based gene expression analysis.Neurobiology of aging · 2020Article
- Peri-arterial pathways for clearance of α-Synuclein and tau from the brain: Implications for the pathogenesis of dementias and for immunotherapy.Alzheimer's & dementia (Amsterdam, Netherlands) · 2020Article
- Antibody-mediated clearance of tau in primary mouse microglial cultures requires Fcγ-receptor binding and functional lysosomes.Scientific reports · 2019Article
- Selective localization of IgG from cerebrospinal fluid to brain parenchyma.Journal of neuroinflammation · 2018Article
- Therapeutic Potential of Intravenous Immunoglobulin in Acute Brain Injury.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
In this study, we investigate the underlying mechanisms of antibody-mediated inflammation in the brain. We show that immune complexes formed in the brain parenchyma generate a robust and long-lasting inflammatory response, characterized by increased expression of the microglia markers CD11b, CD68 and FcRII/III, but no neutrophil recruitment. In addition to these histological changes, we observed transient behavioural changes that coincided with the inflammatory response in the brain. The inflammatory and behavioural changes were absent in Fc-gamma chain (Fcγ)-deficient mice, while C1q-deficient mice were not different from wild-type mice. We conclude that, in the presence of antigen, antibodies can lead to a local immune complex-mediated inflammatory reaction in the brain parenchyma and indirectly induce neuronal tissue damage through recruitment and activation of microglia via Fcγ receptors. These observations may have important implications for the development of therapeutic antibodies directed against neuronal antigens used for therapeutic intervention in neurological diseases.
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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.