Assessment of dectin-2 function on inflammatory cells. Assessment of the impact of blockade of dectin-2 on the recognition (upper graphs) and response to (lower graphs) zymosan of inflammatory neutrophils and monocyte/MØ. Data represents mean±SEM of triplicates from a representative of 3 independent experiments.

Inhibition of dectin-1 and -2-mediated fungal recognition by prior complement opsonization. A) Representative flow cytometric plots of dectin-2 surface expression on NIH3T3 retrovirally transduced with dectin-2 (left panel) and both dectin-2 and FceR chain (right panel). B) Serum-opsonization inhibits the recognition of zymosan by both dectin-1 and dectin-2. NIH3T3 retrovirally transduced as indicated in the legend were incubated with zymosan that had been pre-incubated with serum at increasing concentrations and the interaction was monitored by flow cytometry. Data represents the mean±SEM of triplicates from a representative of 2 independent experiments. Data in (D) was analyzed by two-way ANOVA, with the significant Interaction statistics demonstrating the reduced binding of zymosan to the transduced cells after prior incubation with increasing concentrations of serum.

Assessment of dectin-2 function on inflammatory cells. A) Flow-cytometric plots showing expression of dectin-2 on the surface of inflammatory neutrophils (Ly-6G+) and monocyte/MØ (Ly-6G-). Data is pre-gated on Ly-6B.2+ cells and is representative of results obtained with pooled cells from 3 independent experiments. B) Assessment of the impact of blockade of dectin-2 on the recognition (upper graphs) and response to (lower graphs) zymosan of inflammatory neutrophils and monocyte/MØ from dectin-1-deficient mice. All bars show mean±95% confidence intervals of dectin-2-blocked cells relative to isotype control treated