Tumor Necrosis Factor and Lymphotoxin-Induced Signal Pathways

Tumor necrosis factor (TNF), a cytokine with multiple biological activities, is an important mediator of inflammation and has been recognized as the major pathogenetic factor in sepsis-induced shock and cachexia [1]. Lymphotoxin (LT) binds to the same membrane receptors and exerts a similar, although not identical spectrum of bioactivities [2]. Consistent with TNF/LT’s pleiotropic activities, TNF receptors are expressed on the membrane of virtually all somatic cell types, where they channel signals to the cytoplasm and nucleus to initiate profound alterations in the metabolic state and transcriptional programs of TNF-sensitive cells. We here briefly summarize recent data on the molecular structure of TNF receptors and receptor-induced signal pathways. A detailed review on this subject is given elsewhere [3].