(A) Anti-IgM/CpG-activated or nonactivated B cells were cultivated for 4 h and additionally treated with different concentrations of α1-, α2- or β-ADR agonists for 24 h (n = 6). (B) B cells were either treated with the indicated concentrations of the α2-ADR antagonist RS79948 hydrochloride or with the ß2-ADR antagonist ICI118,551 30 min before activation with anti-IgM/CpG for 24 h (n = 4). (C) B cells were either treated with the β-ADR antagonist nadolol [5μM] 30 min before activation with anti-IgM/CpG or were at first activated with anti-IgM/CpG for 4 h before treating cells with the pan ß-ADR agonist Isopr. (10 μM) (n = 12). The production of IL-10 was analyzed by ELISA (A–C). (D) B cells were cultivated with NE (10 μM), CpG (1.25 μg/ml) or both (CpG+NE) for 4 h. Nontreated B cells were used as control group. The IL-10 mRNA expression was analyzed by qRT-PCR (n = 6). B cells from naive DBA/1J mice were used for the experiments. Data are pooled from 3 (D) or 5 experiments (C). Statistical significance was determined by ordinary 1-way ANOVA followed by Dunnett multiple comparison test (A, B) or Tukey multiple comparison test (C) or Brown–Forsythe and Welch ANOVA test followed by Tamhane T2 multiple comparison test (D). n.s., not significant; *p < 0.5; **p < 0.01; ***p < 0.001; ****p < 0.0001. For underlying data, see S1 Data. ADR, adrenergic receptor; ANOVA, analysis of variance; ELISA, enzyme-linked immunosorbent assay; IL, interleukin; Isopr., isoproterenol; NE, norepinephrine; qRT-PCR, quantitative real-time polymerase chain reaction.