Many cytokines alter the half-lives and stabilities of mRNAs for other cytokines (1 ) and enzymes that may be related to disease progression. For example, IL-1β stabilizes the mRNA for human interstitial collagenase-1 in normal fibroblasts, but not in breast cancer cells (2 ). Altering mRNA stability through direct control of specific RNase activity is a rapid way for cells to respond to environmental changes. Small differences in half-life can have dramatic effects on expressed products; a sixfold increase in μ heavy-chain mRNA half-life in differentiated B-cells largely accounted for a 100-fold increase in its messenger concentration compared to the undifferentiated cells (3 ). The high specific activity of RNases makes them ideal cellular targets for interaction with cytokines (4 ).
