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ScopeArabinoxylan is one of the most commonly consumed dietary fiber. Immunomodulation by arabinoxylan is documented but the mechanisms by which these immune-effects are accomplished are unknown.Methods and resultsBy applying reporter cell lines for Toll-like receptors (TLRs) and Dectin-1, we demonstrated that arabinoxylan interacts with Dectin-1 receptors and not with TLRs. Arabinoxylan activates Dectin-1 to a similar magnitude as soluble -glucans. Soluble beta-glucans are known to inhibit the particulate beta-glucan-induced activation of Dectin-1. As arabinoxylan is also soluble, the inhibiting capacity of arabinoxylan on particulate -glucan-activated Dectin-1 cell lines was studied. It was found that this inhibition was similar to that of soluble -glucan and was caused predominantly by inhibition of the Dectin-1A transcript variant. The Dectin-1 inhibitory function of arabinoxylan was further confirmed in human dendritic cells that demonstrated reduced production of IL-10 and TNF-alpha The production of the antifungal cytokines IL-4 and IL-23 were increased in dendritic cells stimulated with arabinoxylan and particulate -glucan. In contrast to soluble -glucan, arabinoxylan did not enhance production of IL-10, TNF-alpha, and IL-23.ConclusionArabinoxylan activates Dectin-1 and supports antifungal immune responses in human dendritic cells. The mode of action of arabinoxylan is similar but not identical to that of soluble beta-glucans.