ArticleNeuropathology and applied neurobiology2021
Balloon cells promote immune system activation in focal cortical dysplasia type 2b.
Article in Neuropathology and applied neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.
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Who cites it
28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.
- Meta-analysis of treatment-emergent seizures in glioma vaccine trials.Journal of neuro-oncology · 2026Pooled it
- Molecular Signature in Focal Cortical Dysplasia: A Systematic Review of RNA and Protein Data.International journal of molecular sciences · 2025Pooled it
- Focal Cortical Dysplasia Type II: Somatic Mutations, Molecular Mechanisms, and Integrative Multi-Omics Framework.CNS neuroscience & therapeutics · 2026Review
- Plasma extracellular vesicles-derived microRNAs provide potential biomarkers in distinguishing between focal cortical dysplasia type I and II.Pediatric research · 2026Article
- CX3CL1/CX3CR1 axis dysregulation contributes to epileptogenic mechanisms in focal cortical dysplasia.Acta neuropathologica communications · 2026Article
- Beyond mTOR: Unraveling the Complex Pathophysiology and Signaling Pathways in Focal Cortical Dysplasia.Molecular neurobiology · 2025Review
- Single-cell genotyping and transcriptomic profiling of mosaic focal cortical dysplasia.Nature neuroscience · 2025Article
- The Role of Neuroinflammation and Network Anomalies in Drug-Resistant Epilepsy.Neuroscience bulletin · 2025Review
- Multimodal single-cell analyses reveal molecular markers of neuronal senescence in human drug-resistant epilepsy.The Journal of clinical investigation · 2025Article
- Focal cortical dysplasia type II: review of neuropathological manifestations and pathogenetic mechanisms.Acta epileptologica · 2025Review
- Multimodal single-cell profiling reveals neuronal vulnerability and pathological cell states in focal cortical dysplasia.iScience · 2024Article
- Spatial transcriptomics in focal cortical dysplasia type IIb.Acta neuropathologica communications · 2024Article
- [(Auto)immunity in focal epilepsy: mechanisms of (auto‑)immune-inflammatory epileptogenic neurodegeneration].Der Nervenarzt · 2024Review
- Balloon cells in malformations of cortical development: friends or foes?Acta epileptologica · 2024Review
- Analysis of clinical characteristics and histopathological transcription in 40 patients afflicted by epilepsy stemming from focal cortical dysplasia.Epilepsia open · 2024Article
- mTOR and neuroinflammation in epilepsy: implications for disease progression and treatment.Nature reviews. Neuroscience · 2024Review
- CNS autoimmune response in the MAM/pilocarpine rat model of epileptogenic cortical malformation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Identification of gene regulatory networks affected across drug-resistant epilepsies.Nature communications · 2024Article
- Functional profile of perilesional gray matter in focal cortical dysplasia: an fMRI study.Frontiers in neuroscience · 2024Article
- Iconography of abnormal non-neuronal cells in pediatric focal cortical dysplasia type IIb and tuberous sclerosis complex.Frontiers in cellular neuroscience · 2024Review
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Authors and funding
17 authors at 8 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsFocal cortical dysplasia (FCD) type 2 is an epileptogenic malformation of the neocortex associated with somatic mutations in the mammalian target of rapamycin (mTOR) pathway. Histopathologically, FCD 2 is subdivided into FCD 2a and FCD 2b, the only discriminator being the presence of balloon cells (BCs) in FCD 2b. While pro-epileptogenic immune system activation and inflammatory responses are commonly detected in both subtypes, it is unknown what contextual role BCs play.
methodsThe present study employed RNA sequencing of surgically resected brain tissue from FCD 2a (n = 11) and FCD 2b (n = 20) patients compared to autopsy control (n = 9) focusing on three immune system processes: adaptive immunity, innate immunity and cytokine production. This analysis was followed by immunohistochemistry on a clinically well-characterised FCD 2 cohort.
resultsDifferential expression analysis revealed stronger expression of components of innate immunity, adaptive immunity and cytokine production in FCD 2b than in FCD 2a, particularly complement activation and antigen presentation. Immunohistochemical analysis confirmed these findings, with strong expression of leukocyte antigen I and II in FCD 2b as compared to FCD 2a. Moreover, T-lymphocyte tissue infiltration was elevated in FCD 2b. Expression of markers of immune system activation in FCD 2b was concentrated in subcortical white matter. Lastly, antigen presentation was strongly correlated with BC load in FCD 2b lesions.
conclusionWe conclude that, next to mutation-driven mTOR activation and seizure activity, BCs are crucial drivers of inflammation in FCD 2b. Our findings indicate that therapies targeting inflammation may be beneficial in FCD 2b.
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