Supplementary Figures S1-S10 from TLR Signaling Is Activated in Lymph Node–Resident CLL Cells and Is Only Partially Inhibited by Ibrutinib

Supplementary Figure S1: Dose response experiments with the IRAK1/4 inhibitor (IRAKi) in CLL cells. Supplementary Figure S2: TLR signaling is active in lymph node-resident CLL cells. Supplementary Figure S3: Flow Cytometry gating strategy. Supplementary Figure S4: Early activation of STAT3 leads to early production of serum IL-10. Supplementary Figure S5: TLR signaling induces similar levels of IRAK1 degradation and STAT signaling in vitro with CpG stimulation in primary CLL PBMCs. Supplementary Figure S6: Upstream IRAK1 degradation and downstream phosphorylation of STAT3 and IκBα are inversely related. Supplementary Figure S7: CpG induced TLR signaling promotes cell survival and activates CLL cells in vitro. Supplementary Figure S8: Inhibiting induced TLR activation downregulates expression of activation markers and prevents the survival advantage in CLL cells. Supplementary Figure S9: αIgM stimulation induces activation of BCR pathway signaling. Supplementary Figure S10: Ibrutinib inhibits both BCR and TLR signaling in activated CLL cells harvested from the lymph node.