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. 2013 Jan 4;25(5):295–306. doi: 10.1093/intimm/dxs114

Fig. 3.

Fig. 3.

Relative contributions of IRF5 and the DOCK2 mutation to B-cell IL-6 production and proliferation. (A and B) B cells were purified from the spleens of Jackson C57BL/6 wild-type mice, IRF5 −/− 14G mice and IRF5 −/− 11G mice (with the DOCK2 mutation) using CD23-positive selection. (A) The B cells were stained with antibodies against B220, AA4.1, IgM, CD21 and CD23. Data are representative of three independent experiments. IM, immature B cells; M, mature B cells; T, transitional B cells; MZ, marginal zone B cells; FO, follicular B cells. (B) B cells were stimulated with LPS (30 µg/ml), Pam3Cys (1 µg/ml), 1826 and CL097 for 48h in the presence of BLyS (50ng/ml). IL-6 levels in the supernatants were measured by ELISA. The data represent the mean ± SEM of three independent experiments. **P < 0.01; ***P < 0.001 versus IRF5+/+. There was no statistical difference between B cells from IRF5 −/− 14G and IRF5 −/− 11G mice. (C) B cells were purified from the spleens of Jackson C57BL/6 wild-type mice (n = 3), IRF5 +/+ (n = 5) and IRF5 −/− (n = 3) 15G littermates, and IRF5 −/− 11G mice (with the DOCK2 mutation) (n =6) using CD23-positive selection. The B cells were stimulated with 1826 (3 µg/ml), CL097 (3 µg/ml), LPS (30 µg/ml), Pam3Cys (1 µg/ml) and anti-IgM antibody (30 µg/ml) for 42h in the presence of BLyS (50ng/ml) and pulsed with 3H thymidine for 6h. The data represent the mean ± SEM of three independent experiments.