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. Author manuscript; available in PMC: 2018 May 15.
Published in final edited form as: Clin Cancer Res. 2016 Oct 25;23(10):2506–2515. doi: 10.1158/1078-0432.CCR-16-1996

Figure 2.

Figure 2

TCR engagement activates NF-κB and confers resistance to chemotherapy in T-cell lymphomas. (A) NF-κB (p65) was examined in nuclear extracts following bead stimulation in T8ML-1 and primary TCL cells. Representative western blots are shown. (B) Nuclear NF-κB (p65) DNA binding was determined following bead stimulation by ELISA in conventional T-cells (“T-cell”), in T8ML-1 and in primary TCL cells (n=4). (C) Expression of selected NF-κB target genes (NFκB1A, IL2Rα, TNF) was examined by qRT-PCR following bead stimulation. The relative increase (compared with unstimulated cells) in mRNA for normal T cells, T8ML-1, and primary TCL cells (n=2) is shown. (D) T8ML-1 cells and primary TCL specimens (n=3) were cultured with romidepsin (2 nM) or vincristine (6 nM) in the presence or absence of CD3/CD28 beads, as indicated, and cell viability determined 48 hours later in a standard MTT assay and reported as relative to control cells (neither treated with CD3/CD28 beads nor chemotherapy). (*p<0.05, **p<0.01, ***p<0.001)