{Reference Type}: Journal Article
{Title}: Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID-19-associated Guillain-Barré syndrome.
{Author}: Li Z;Huang Z;Li X;Huang C;Shen J;Li S;Zhang L;Wong SH;Chan MTV;Wu WKK;
{Journal}: Cell Prolif
{Volume}: 54
{Issue}: 5
{Year}: May 2021
{Factor}: 8.755
{DOI}: 10.1111/cpr.13024
{Abstract}: <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.