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10.1111/cpr.13024

http://scihub22266oqcxt.onion/10.1111/cpr.13024
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33751722!8088459!33751722
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suck abstract from ncbi


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pmid33751722      Cell+Prolif 2021 ; 54 (5): e13024
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  • Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID-19-associated Guillain-Barre syndrome #MMPMID33751722
  • Li Z; Huang Z; Li X; Huang C; Shen J; Li S; Zhang L; Wong SH; Chan MTV; Wu WKK
  • Cell Prolif 2021[May]; 54 (5): e13024 PMID33751722show ga
  • OBJECTIVES: Guillain-Barre 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 METHODS: We performed bioinformatic analyses to delineate the potential genetic crosstalk between COVID-19 and GBS. RESULTS: COVID-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. CONCLUSIONS: Augmented 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.
  • |B7-2 Antigen/metabolism[MESH]
  • |COVID-19/complications/*pathology/virology[MESH]
  • |Cell Differentiation[MESH]
  • |Computational Biology/*methods[MESH]
  • |Cytokines/*metabolism[MESH]
  • |Gene Regulatory Networks[MESH]
  • |Guillain-Barre Syndrome/etiology/metabolism/*pathology[MESH]
  • |Humans[MESH]
  • |Interleukin-23 Subunit p19/metabolism[MESH]
  • |Leukocytes, Mononuclear/cytology/metabolism[MESH]
  • |Protein Interaction Maps[MESH]
  • |SARS-CoV-2/isolation & purification[MESH]
  • |Signal Transduction[MESH]


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