ArticleScientific reports2017
Uniting the neurodevelopmental and immunological hypotheses: Neuregulin 1 receptor ErbB and Toll-like receptor activation in first-episode schizophrenia.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Monocytic TLR4 expression and activation in schizophrenia: A systematic review and meta-analysis.PloS one · 2025Pooled it
- Serum TLR4, NF-κB, and NLRP3 Levels in Children with Attention-Deficit/Hyperactivity Disorder: A Case-Control Study.Children (Basel, Switzerland) · 2026Article
- Gene expression changes in Brodmann's Area 46 differentiate epidermal growth factor and immune system interactions in schizophrenia and mood disorders.Schizophrenia (Heidelberg, Germany) · 2024Article
- The Emerging Role of Toll-Like Receptor-Mediated Neuroinflammatory Signals in Psychiatric Disorders and Acquired Epilepsy.Molecular neurobiology · 2024Review
- Counting the Toll of Inflammation on Schizophrenia-A Potential Role for Toll-like Receptors.Biomolecules · 2023Review
- Toll-Like Receptor (Neuropsychiatric disease and treatment · 2023Article
- Peripheral NF-κB dysregulation in people with schizophrenia drives inflammation: putative anti-inflammatory functions of NF-κB kinases.Translational psychiatry · 2022Article
- Monocytic Subsets Impact Cerebral Cortex and Cognition: Differences Between Healthy Subjects and Patients With First-Episode Schizophrenia.Frontiers in immunology · 2022Article
- Alterations in innate immune defense distinguish first-episode schizophrenia patients from healthy controls.Frontiers in psychiatry · 2022Article
- Neuroinflammation in schizophrenia: the role of nuclear factor kappa B.Translational psychiatry · 2021Review
- The RTK Interactome: Overview and Perspective on RTK Heterointeractions.Chemical reviews · 2019Review
- CaMKIIα expression in a mouse model of NMDAR hypofunction schizophrenia: Putative roles for IGF-1R and TLR4.Brain research bulletin · 2018Article
- Changed frontal pole gene expression suggest altered interplay between neurotransmitter, developmental, and inflammatory pathways in schizophrenia.NPJ schizophrenia · 2018Article
- Low Field Magnetic Stimulation Ameliorates Schizophrenia-Like Behavior and Up-Regulates Neuregulin-1 Expression in a Mouse Model of Cuprizone-Induced Demyelination.Frontiers in psychiatry · 2018Article
- Peripheral Transcription ofFrontiers in psychiatry · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current pathophysiological models of schizophrenia focus on neurodevelopmental and immunological mechanisms. We investigated a molecular pathway traditionally linked to the neurodevelopmental hypothesis (neuregulin 1 - ErbB), and pathogen-associated pattern recognition receptors associated with the immune hypothesis (Toll-like receptors, TLRs). We recruited 42 first-episode, drug-naïve patients with schizophrenia and 42 matched healthy control subjects. In monocytes TLR4/TLR5 and ErbB expressions were measured with flow-cytometry. Pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) and the anti-inflammatory cytokine IL-10 were determined following the stimulation of TLR4/TLR5 and ErbB. Results revealed increased TLR4/TLR5 and decreased ErbB4 expression in schizophrenia relative to the control subjects. The expression of ErbB2 and ErbB3 receptors was unaltered in schizophrenia. TLR4 stimulation resulted in lower pro-inflammatory cytokine production in schizophrenia compared to the control levels, whereas the stimulation of ErbB by neuregulin 1 led to higher pro-inflammatory cytokine levels in patients with schizophrenia relative to the control group. In healthy controls, ErbB activation was associated with a marked production of IL-10, which was dampened in schizophrenia. These results indicate that the stimulation of TLR4 and ErbB induces opposite pro-inflammatory cytokine responses in schizophrenia.
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