%0 Journal Article
%T Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID-19-associated Guillain-Barré syndrome.
%A Li Z
%A Huang Z
%A Li X
%A Huang C
%A Shen J
%A Li S
%A Zhang L
%A Wong SH
%A Chan MTV
%A Wu WKK
%J Cell Prolif
%V 54
%N 5
%D May 2021
%M 33751722
%F 8.755
%R 10.1111/cpr.13024
%X <B>OBJECTIVE: </B>Guillain-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.<BR><B>METHODS: </B>We performed bioinformatic analyses to delineate the potential genetic crosstalk between COVID-19 and GBS.<BR><B>RESULTS: </B>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.<BR><B>CONCLUSIONS: </B>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.