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Journal of Experimental Medicine, Vol 173, 699-703, Copyright © 1991 by Rockefeller University Press
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EP Sampaio, EN Sarno, R Galilly, ZA Cohn and G Kaplan
Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.
Thalidomide selectively inhibits the production of human monocyte tumor necrosis factor alpha (TNF-alpha) when these cells are triggered with lipopolysaccharide and other agonists in culture. 40% inhibition occurs at the clinically achievable dose of the drug of 1 micrograms/ml. In contrast, the amount of total protein and individual proteins labeled with [35S]methionine and expressed on SDS-PAGE are not influenced. The amounts of interleukin 1 beta (IL-1 beta), IL-6, and granulocyte/macrophage colony-stimulating factor produced by monocytes remain unaltered. The selectivity of this drug may be useful in determining the role of TNF-alpha in vivo and modulating its toxic effects in a clinical setting.
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