CD4 and Guillain-Barre syndrome: While these findings are consistent with EAN being predominantly a Th1 cell-mediated autoimmune peripheral nerve disorder, the pathogenesis of Guillain-Barré Syndrome (GBS) most likely involves an imbalance between pro-inflammatory (Th1, Th17) and anti-inflammatory (Th2, T regulatory) subsets of CD4+ T cells (Zhang et al., 2013).