INTERLEUKIN-1 INDUCTION OF TUMOR-NECROSIS-FACTOR-ALPHA MESSENGER-RNA AND BIOACTIVE TUMOR-NECROSIS-FACTOR-ALPHA IN A PANCREATIC BETA-CELL LINE BY A MECHANISM REQUIRING NO DE-NOVO PROTEIN-SYNTHESIS

Interleukin-1 (IL-1) has been implicated as an effector in insulitis of Type 1 (insulin-dependent) diabetes. Exposure of a β-cell line TC1) to IL-1β resulted in an increase of preproinsulin mRNA at 0.5 h followed by a gradual decrease. Tumor necrosis factor-α (TNF-α) mRNA expression by βTC1 cells was demonstrated 1-3 h after the addition of IL-1β. TNF bioactivity was detected in homogenates of βTC1 cells exposed of IL-1. The supplementation of cycloheximide (CHX) together with IL-1β resulted in the superinduction of TNF-α mRNA, suggesting that de novo protein synthesis is not required in IL-1-induced TNF-α mRNA expression. Endogenous TNF-α of β-cells may be involved in the islet lesion of type 1 diabetes. © 1993 Academic Press, Inc.