Recognition of alpha-mannan by dectin 2 is essential for onset of Kawasaki disease-like murine vasculitis induced by Candida albicans cell-wall polysaccharide

Objectives: Using a murine model of systemic Kawasaki disease (KD)-like vasculitis induced by Candida albicans cell-wall-derived mannan center dot beta-glucan center dot protein complexes, the objective was to elucidate the relationships of beta-glucan receptor dectin-1 (D1) and alpha-mannan receptor dectin-2 (D2) to the onset of that vasculitis. Methods: The incidence and histological severity of vasculitis were compared among mice lacking the genes for D1 or D2 (i.e. D1(-/-) and D2(-/-)) and wild-type (WT) mice. Results: The incidences of vasculitis in the three animal groups were 100% (18/18) in the WT group, 100% (18/18) in the D1(-/-) group, and 0% (0/18) in the D2(-/-) group. In the WT and D1(-/-) mice, severe inflammatory cell infiltration, consisting mainly of neutrophils and macrophages, was seen in the aortic root and the coronary arteries. On the other hand, in the D2(-/-) mice, not even mild vascular lesions such as endoarteritis were seen. Conclusion: Recognition of alpha-mannan by D2 played an important role in the onset of vasculitis in the studied murine model.