TLR triggering specifically induces multiple antiapoptotic molecules in pDCs. Quantitative RT-PCR of antiapoptotic genes, BCL2L1, BCL2, BIRC3, and CFLAR (A), and proapoptotic genes, CASP-8, BID, BAX, and BAD (B). For each donor the condition with the highest relative expression was set to 100%. Experiments were performed on freshly purified pDCs (ex vivo) or after 6 hours of culture in the presence of medium alone (Med), IL3 (IL-3), Flu, IFN-α, TNF-α, and IFN-α plus TNF-α (A-B). Planar representation of proapoptotic versus antiapoptotic balance in stimulated pDCs (C). To compress the data, one vector x = (BCL2L1 = Bcl-XL, Bcl2, BIRC3 = iap2, CFLAR = c-flip) of antiapoptotic markers, and another vector y = (CASP8 = caspase-8, BID, BAX, BAD) of proapoptotic markers were defined. Then, Euclidean length was computed using the percentage values donor by donor. For each culture condition, the corresponding point is the mean length of 3 independent donors. The error bars correspond to the SDs. Quantitative RT-PCR of antiapoptotic genes, BCL2L1, BCL2, BIRC3, and CFLAR, of Flu-stimulated pDCs in the presence of blocking IFN-α, TNF-α, or both (D). The mean and SD of 3 independent donors are represented. Differential expression between conditions was assessed by Student t test (NS, not significant; *P < .05; **P < .01).