Functional antagonism by GM-CSF on TNF-α-induced CD83 expression in human neutrophils

Our results show that co-stimulation with pro-inflammatory cytokines such as TNFα and GM-CSF can have differential effects on inflammatory pathways initiated in the same target cell. GM-CSF can both synergize with TNFα in the case of expression of IL1-RA and antagonize in the case of CD83. Therefore, expression of CD83 as read out for activation of neutrophils in patients with inflammatory diseases is complicated by the presence of cross-modulating cytokines such as GM-CSF.