Figure 1. β-Glucan treatment converts M2 macrophage characteristic gene expression and its immunosuppressive function and activates Syk/Erk in a dectin-1-dependent manner.

(A) Polarized M2 BMM from WT mice (n=3) were treated with WGP β-glucan for 6 h. The total RNAs were extracted for the microarray analysis. (B) mRNA expression levels of specific genes as indicated in polarized M2 BMM from WT, CD11b^−/− or dectin-1^−/− mice upon stimulation with WGP β-glucan by quantitative real-time (qRT) PCR. (C) Splenocytes from OVA Tg OT-I and OT-II mice were labeled with CFSE and then stimulated with OVA in the presence of polarized M2 BMM (ratio 1:20) with or without WGP β-glucan treatment. Histogram shows cell proliferation. (D) Polarized M2 BMM from WT, CD11b^−/− or Dectin-1^−/− mice were stimulated with WGP β-glucan at indicated time points. Cells were lysed and extracted proteins were probed with Abs to p-Stat3, p-Akt, p-P38, pZap/Syk, p-Erk1/2, and β-actin. (E) M2 BMM were stimulated with WGP β-glucan in the presence or absence of the Syk inhibitor. The expression of p-Syk and p-Erk1/2 was determined by WB. (F) M2 BMM from WT or Card9 KO mice were treated with or without WGP β-glucan at indicated time points. Lysates were immunoblotted with p-Erk1/2, Erk1/2, and β-actin Abs. Data are representative of three independent experiments with similar results. *P<0.05, **P<0.01.