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. Author manuscript; available in PMC: 2015 Jul 15.
Published in final edited form as: J Immunol. 2014 Jun 13;193(2):519–528. doi: 10.4049/jimmunol.1301668

Figure 6. Redirected killing: human CTL utilize secretory granule and Fas-mediated pathways to activate Caspase 3/7 in target cells conjugated by anti-CD3.

Figure 6

(A) HVS transformed human CTL were co-incubated at 1:1 with GLS.DEVD expressing, cloned P815 cells, pre-incubated with anti-CD3 antibody. P815 cells without added effectors are shown as a negative control. Evaluation of RLU out to 240 minutes reveals early activation of GLS.DEVD in P815 incubated with wild type (wt) CTL contrasting with (B) late activation following co-incubation with perforin deficient CTL (Prf −/−). The early activation in the wt cell line was prevented by the addition of concanamycin A (CMA) but not brefeldin (BFA), demonstrating the dependence upon the secretory granule pathway. Addition of anti-FasL antibody to the PRF −/− CTL prevented the delayed rise in GLS.DEVD (B) confirming the role of the delayed onset death receptor pathway. Shown is a representative figure from 3 independent experiments utilizing these two HVS lines.