The axonal subtype of GBS is closely associated with antecedent CJ infection and the lipopolysaccharides (LPS) of CJ can induce the production of anti-GM1 and anti-GQ1b antibodies in animal models.[3,41] As shown in the study by Vigne et al, LPS can significantly stimulate the expression of IL-36α and IL-36γ in bone marrow-derived DCs, while the expression of IL-36β and IL-36Ra is not remarkably increased.[25] We postulate that LPS from CJ may also be involved in the pathogenesis of GBS, leading to increased serum IL-36α and IL-36γ levels. This evidence concerns the gene IL36B and Guillain-Barre syndrome.