Abstract
Tumor necrosis factor (TNF) was initially described in the sera of Mycobacterium bovis strain BCG infected mice treated with endotoxin (2) and defined by its ability to cause necrosis of tumors in mice. In addition to this potentially beneficial effect, TNF has been shown to be intimately involved in the pathophysiology of bacterial lipopolysaccharide (LPS)-induced shock and lethality in mice (1). In both instances, the primary sources of TNF are macrophages (5).
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References
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Birkland, T.P., Cornwell, R.D., Golenbock, D.T., Proctor, R.A. (1990). Comparative Study of Lipopolysaccharide-, Lipid IVa-, and Lipid X-Induced Tumor Necrosis Factor Production in Murine Macrophage-Like Cell Lines. In: Friedman, H., Klein, T.W., Nakano, M., Nowotny, A. (eds) Endotoxin. Advances in Experimental Medicine and Biology, vol 256. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-5140-6_35
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DOI: https://doi.org/10.1007/978-1-4757-5140-6_35
Publisher Name: Springer, Boston, MA
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