Table I.

Effect of death inhibitors on CTL AICD

Inhibitor TypeInhibitora% AICD Inhibitionbpc
CaspasesBOC-D-FMK43.6 ± 11.60.001*
ZVAD-FMK27.9 ± 10.10.002*
Fas/FasLAnti-FasL36.9 ± 13.20.001*
Fas:Fc35.9 ± 12.80.006*
NAC7.5 ± 1.90.01*
TNFα/TNFRAnti-TNFα7.4 ± 8.30.3
TNFR-Fc−2.0 ± 1.10.15
TRAIL/TRAILR23.2 ± 16.50.07
O2/N2 RadicalsMnTBAP7.0 ± 4.10.04*
BHA1.9 ± 6.60.9
L-NMMA−2.4 ± 1.30.4
  • a ZVAD- and BOC-D-FMK are broad-spectrum CI. Anti-FasL (MFL3) and anti-TNFα (TN3 19.12) are neutralizing monoclonal Abs. Fas-Fc, TNFR-Fc and TRAILR-Fc are soluble fusion proteins with neutralizing activity towards FasL, TNF-α, and TRAIL respectively. NAC is an antioxidant known to reduce levels of FasL on T cells. MnTBAP is a superoxide dismutase mimetic and peroxynitrite scavenger. L-NMMA is a competitive inhibitor of nitric oxide synthase. Butylated hydroxyanisole is a phenolic antioxidant known to protect against TNF-α-mediated cytotoxicity. In each case, CTL were preincubated with the inhibitors for 2 h prior to overnight incubation in the presence of Kb-OVA257–264.

  • b Percentage inhibition of AICD is determined as follows: (100 − (monomer-induced death with inhibitor/monomer-induced death without inhibitor) × 100. Numbers represent the average of triplicate samples ± SD of the mean.

  • c Values of p were calculated using Student’s t test. Reagents that significantly blocked CTL death (p < 0.05) are marked with an asterisk. The table lists combined results from at least four experiments per inhibitor.