ArticleCell proliferation2021
Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID-19-associated Guillain-Barré syndrome.
Article in Cell proliferation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Sinomenine ameliorates experimental autoimmune neuritis by suppressing pro-inflammatory immune components and restoring immune balance.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Identifying potential co-expressed genes and molecular mechanisms linking post-COVID-19 and Guillain-Barre syndrome through neutrophil extracellular trap-related genes.Frontiers in neurology · 2025Article
- Identification of immune-related hub genes and potential molecular mechanisms involved in COVID-19 via integrated bioinformatics analysis.Scientific reports · 2024Article
- Advances in Exosome-Based Therapies for the Repair of Peripheral Nerve Injuries.Neurochemical research · 2024Review
- Is there a causal nexus between COVID-19 infection, COVID-19 vaccination, and Guillain-Barré syndrome?European journal of medical research · 2023Review
- Simulation of COVID-19 symptoms in a genetically engineered mouse model: implications for the long haulers.Molecular and cellular biochemistry · 2023Article
- Auto-immunoproteomics analysis of COVID-19 ICU patients revealed increased levels of autoantibodies related to the male reproductive system.Frontiers in physiology · 2023Article
- Immune repertoire analysis of normal Chinese donors at different ages.Cell proliferation · 2022Article
- Relationship Between Acute Phase Reactants and Disability in Guillian-Barré Syndrome During the COVID-19 Pandemic.Archives of medical research · 2022Article
- Molecular docking and molecular dynamics study Lianhua Qingwen granules (LHQW) treats COVID-19 by inhibiting inflammatory response and regulating cell survival.Frontiers in cellular and infection microbiology · 2022Article
- Discovering common pathogenetic processes between COVID-19 and sepsis by bioinformatics and system biology approach.Frontiers in immunology · 2022Article
- Maternal Immune Activation and Interleukin 17A in the Pathogenesis of Autistic Spectrum Disorder and Why It Matters in the COVID-19 Era.Frontiers in psychiatry · 2022Article
- Interleukin-17A (IL-17A): A silent amplifier of COVID-19.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Article
- Review
- A Review of Neurological Involvement in Patients with SARS-CoV-2 Infection.Medical science monitor : international medical journal of experimental and clinical research · 2021Review
- Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID-19-associated Guillain-Barré syndrome.Cell proliferation · 2021Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesGuillain-Barré syndrome (GBS) results from autoimmune attack on the peripheral nerves, causing sensory, motor and autonomic abnormalities. Emerging evidence suggests that there might be an association between COVID-19 and GBS. Nevertheless, the underlying pathophysiological mechanism remains unclear. MATERIALS AND
methodsWe performed bioinformatic analyses to delineate the potential genetic crosstalk between COVID-19 and GBS.
resultsCOVID-19 and GBS were associated with a similar subset of immune/inflammation regulatory genes, including TNF, CSF2, IL2RA, IL1B, IL4, IL6 and IL10. Protein-protein interaction network analysis revealed that the combined gene set showed an increased connectivity as compared to COVID-19 or GBS alone, particularly the potentiated interactions with CD86, IL23A, IL27, ISG20, PTGS2, HLA-DRB1, HLA-DQB1 and ITGAM, and these genes are related to Th17 cell differentiation. Transcriptome analysis of peripheral blood mononuclear cells from patients with COVID-19 and GBS further demonstrated the activation of interleukin-17 signalling in both conditions.
conclusionsAugmented Th17 cell differentiation and cytokine response was identified in both COVID-19 and GBS. PBMC transcriptome analysis also suggested the pivotal involvement of Th17 signalling pathway. In conclusion, our data suggested aberrant Th17 cell differentiation as a possible mechanism by which COVID-19 can increase the risk of GBS.
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