These results and previous evidence collectively suggested that IL-36α and IL-36γ may aggravate inflammatory injuries in GBS patients by promoting the secretion of IL-17 and TNF-α.[30,31] Simultaneously, IL-17 and TNF-α may also interact to induce the expression of IL-36α and IL-36γ in GBS. This evidence concerns the gene IL36A and Guillain-Barre syndrome.