Figure 6. Defective STAT3 signalling in c-Abl-deficient PC.

Analyses of various signaling pathways in in vitro generated PC harvested at day 6 of culture. (A) Intracellularly-stained IgG1⁺CD138⁺ PC were examined for their actin structure by co-staining with phalloidin in FACS analysis in control (red histogram) and c-Abl^f/f Aicda^cre/+ mice (blue histogram). (B) Flow cytometry analysis of soluble VCAM-1-Fc (20 μg/ml) and ICAM-1-Fc (20 μg/ml) binding by in-vitro differentiated cells from control (black columns) and c-Abl^f/f Aicda^cre/+ (white columns) mice. (C) IgG1⁺CD138⁺ PC generated from control and c-Abl^f/f Aicda^cre/+ B cell cultures were examined for levels of STAT1, STAT3 and STAT5 phosphorylation. Quantification of the percentage of phosphorylated STAT1, STAT3 and STAT5 in control (black circles) and c-Abl^f/f Aicda^cre/+ (white circles) PC. (D) ELISPOT and statistical analyses of NP-specific PCs in the spleens of control, c-Abl^f/f Aicda^cre/+, and c-Abl^f/f Aicda^cre/+ mice treated with the STAT3-activator Colivelin. 5 days after NP₃₈-CGG challenge, c-Abl^+/+ Aicda^cre/+ and c-Abl^f/f Aicda^cre/+ mice were injected with the vehicle control saline buffer and/or STAT3 activator Colivelin (dosage at 1.5 μg/g body weight). Each circle represents one set of experiment performed.