Validation of the cells for future applications for drug screening. (A) Inhibition of IL-1β (top panel), IL-6 (middle panel), or IL-8 (bottom panel) secretion from wild-type iPS-MPs by various inhibitors. The iPS-MPs were cultured for 2 hours in the presence of 100μM cycloheximide (CHX), 100μM MG132, 10μM Bay11-7082, 25μM CA074Me, 50μM Ac-YVAD-CHO, as well as 10-fold dilutions of each inhibitor, except CA074Me (which was diluted 5-fold), followed by LPS treatment plus ATP stimulation. n = 3. (B) The differential inhibition of IL-1β secretion from wild-type iPS-MPs by various inhibitors. In the presence of inhibitors, such as PPADS (300μM), CA074Me (25μM), or Ac-YVAD-CHO (50μM), LPS-primed wild-type iPS-MPs were stimulated with second signal triggers, such as ATP for 1 hour (top panel), silica crystals for 1 hour (middle panel), or monosodium urate crystals for 3 hours (bottom panel). n = 3. (C) Inhibition of IL-1β (top panel), IL-6 (middle panel), or IL-8 (bottom panel) secretion from mutant iPS-MPs by various inhibitors was evaluated as in panel A; n = 3. (D) Inhibition of IL-1β secretion from mutant iPS-MPs by various inhibitors. In the presence of inhibitors, such as PPADS (300μM), CA074Me (25μM), or Ac-YVAD-CHO (50μM), mutant iPS-MPs were stimulated with LPS for 4 hours. n = 3. Data are mean ± SEM. ***P < .001 (Student t test). **P < .01 (Student t test). *P < .05 (Student t test).