Figure 6
Figure 6. Btk and PLC-γ2 phosphorylation inhibition in B-cell subsets. (A) Btk phosphorylation in B-cell subsets cultured in the presence or absence of 10 μM of imatinib, 100 nM of dasatinib, or 10 μM of nilotinib for 2 hours and stimulated with 10 μg/mL of anti-human IgG and IgM F(ab')2 for 20 minutes. Effect of the TKI on pBtk inhibition is shown in gated IgM memory B-cell, switched memory B-cell, and naive B-cell subsets. Each experiment was performed a minimum of 3 times. (B) MFI of BTK phosphorylation in gated CD19+ B cells from a representative healthy donor following incubation with 10 μM of imatinib, 100 nM of dasatinib, or 10 μM of nilotinib.

Btk and PLC-γ2 phosphorylation inhibition in B-cell subsets. (A) Btk phosphorylation in B-cell subsets cultured in the presence or absence of 10 μM of imatinib, 100 nM of dasatinib, or 10 μM of nilotinib for 2 hours and stimulated with 10 μg/mL of anti-human IgG and IgM F(ab')2 for 20 minutes. Effect of the TKI on pBtk inhibition is shown in gated IgM memory B-cell, switched memory B-cell, and naive B-cell subsets. Each experiment was performed a minimum of 3 times. (B) MFI of BTK phosphorylation in gated CD19+ B cells from a representative healthy donor following incubation with 10 μM of imatinib, 100 nM of dasatinib, or 10 μM of nilotinib.

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