Interleukin-1 and Its Biologically Related Cytokines

Interleukin-1 (IL-1) and tumor necrosis factor (TNF) participate in self-augmentation induction mechanisms in cultured cells stimulated with viruses, bacterial toxins, and active complement components, and of immune complex.

Abstract

Interleukin-1 (IL-1) and tumor necrosis factor (TNF) participate in self-augmentation induction mechanisms. Recombinant human IL-1 and TNF are each capable of inducing the production of their respective molecules as well as each other. IL-1 and TNF both induce IL-6. The target cells include: monocytes, endothelial cells, smooth muscle cells, and B cells. The concentrations of IL-1 and TNF that stimulate their own production in this self amplification cycle are within the range (1-10 ng/ml) of what has been measured in the supernatant media of cultured cells stimulated with viruses, bacterial toxins, and active complement components, and of immune complex. The ability of interferon-y to suppress IL-l-induced IL-1 production takes place in the presence of cyclo-oxygenase inhibition. Similarly, the ability of corticosteroids to reduce the transcription of IL-1 messenger RNA (mRNA) also takes place in the presence of cyclooxygenase inhibition. IL-1 is the prototype of a group of biologically potent polypeptides with molecular weights between 10,000 and 30,000. Because these substances are produced by a variety of cells and act on many different cell types, there is a growing acceptance of the terminology "cytokines," rather than "lymphokines" or "monokines." Of the various "cytokines," several share the ability to stimulate or augment cell proliferation, initiate the synthesis of new proteins in a variety of cells, and induce the production of inflammatory metabolites. IL-1 is biologically similar to tumor necrosis factor (TNF), lymphotoxin, IL-6, fibroblast growth factor (FGF), platelet derived growth factor (PDGF), and transforming growth factor- β (TGF-β)