Cachectin/tumor necrosis factor: An endogenous mediator of shock and inflammation

During the past 3 years, cachectin (TNF) has come to be regarded as a proximal mediator of inflammation, which exerts powerful effects on the metabolic activities of host tissues during infection. In the future, it is anticipated that a growing understanding of cachectin and its role in mammalian physiology will yield important advances in basic and clinical science. A precise knowledge of the hormone's mechanism of action may shed light on the causes of inflammation, its benefits and its liabilities. The unusual ability of cachectin to lyse tumor cells in vitro may ultimately lead to the design of effective antineolastic agents. Finally, the molecular events involved that govern the induction of cachectin gene expression by LPS may prove to be very general. Thus, studies of cachectin gene expression may lead to a broader understanding of the central mechanisms by which transcription and translation are effected in mammalian cells.