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 β‐glucans. Soluble β‐glucans are known to inhibit the particulate β‐glucan‐induced activation of Dectin‐1. As arabinoxylan is also soluble, the inhibiting capacity of arabinoxylan on particulate β‐glucan‐activated Dectin‐1 cell lines was studied. It was found that this inhibition was similar to that of soluble β‐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‐α. The production of the antifungal cytokines IL‐4 and IL‐23 were increased in dendritic cells stimulated with arabinoxylan and particulate β‐glucan. In contrast to soluble β‐glucan, arabinoxylan did not enhance production of IL‐10, TNF‐α, 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 β‐glucans.