Figure 4.
Figure 4. Loss of NF-κB activity in DCs converts antiapoptotic signals to proapoptotic signals. (A-C) DCs were transfected with pIRES2-EGFP or IκBαAA-pIRES2-EGFP, and CD1a+/EGFP+ DCs were FACS-sorted. (A) DCs were cultured without stimulants, and viable cells were enumerated at the indicated time points of culture. (B) DCs were cultured in the presence or absence of CD40L, CD95L, or TRAIL. (C) Native or sAg-pulsed DCs were cultured in the presence of autologous T cells or CD40L. (B-C) Viable DCs were enumerated on d15 of culture. Results are presented as percentage of viable DCs after culture relative to the number of input DCs (mean ± SD of triplicate determinations) (A) or as x-fold alteration of survival (mean ± SD of triplicate experiments) relative to the survival of vector-transfected DCs cultured in medium only (B-C). Results are representative of at least 3 independent experiments.

Loss of NF-κB activity in DCs converts antiapoptotic signals to proapoptotic signals. (A-C) DCs were transfected with pIRES2-EGFP or IκBαAA-pIRES2-EGFP, and CD1a+/EGFP+ DCs were FACS-sorted. (A) DCs were cultured without stimulants, and viable cells were enumerated at the indicated time points of culture. (B) DCs were cultured in the presence or absence of CD40L, CD95L, or TRAIL. (C) Native or sAg-pulsed DCs were cultured in the presence of autologous T cells or CD40L. (B-C) Viable DCs were enumerated on d15 of culture. Results are presented as percentage of viable DCs after culture relative to the number of input DCs (mean ± SD of triplicate determinations) (A) or as x-fold alteration of survival (mean ± SD of triplicate experiments) relative to the survival of vector-transfected DCs cultured in medium only (B-C). Results are representative of at least 3 independent experiments.

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