TNF, immunity and inflammatory disease: lessons of the past decade
Beutler, B.
Journal of Investigative Medicine the Official Publication of the American Federation for Clinical Research 43(3): 227-235
1995
ISSN/ISBN: 1081-5589 PMID: 7614068 Document Number: 3567
Tumor necrosis factor (TNF), which was named for its curious ability to trigger necrosis and involution of transplantable tumors, has become known as a central mediator of responses to endotoxin, rheumatoid disease, and other forms of inflammation. It also has been revealed as a vital component of cellular immune defenses against Listeria, mycobacteria, and other intracellular pathogens. The dual character of TNF highlights many aspects of immune system function. Like many important molecules, TNF made its presence known in several ways. Named for its ability to mediate the tumor-necrotizing effect of bacterial endotoxin (lipopolysaccharide [LPS]) in animals with transplantable neoplasms, TNF was found to mediate many other effects of LPS as well. It also has been found to participate in chronic inflammatory disease processes, particularly those depending upon collaboration between T cells and macrophages. Finally, it is clear that TNF is part of a ligand family collectively responsible for a broad range of immunologic and developmental effects. In this review, the key scientific observations that led to our current concept of TNF action are recounted, and an attempt is made to define the role of TNF defense against infection.
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