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March 1, 1991The Journal of Experimental Medicine1,204 citationsOpen Access

Thalidomide selectively inhibits tumor necrosis factor alpha production by stimulated human monocytes.

ESE P SampaioESEuzenir Nunes SarnoRGRuth Galilly

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Abstract

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 35Smethionine 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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Cite This Study

Sampaio et al. (1991) studied this question.

synapsesocial.com/papers/6a10b93cacd1dbe064644ee2https://doi.org/10.1084/jem.173.3.699
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1The complex pattern of cytokines in serum from patients with meningococcal septic shock. Association between interleukin 6, interleukin 1, and fatal outcome.1989 · 1,185 citations
  2. 2Direct stimulation of monocyte release of interleukin 1 by mycobacterial protein antigens.1986 · 88 citations
  3. 3Control of Cachectin (Tumor Necrosis Factor) Synthesis: Mechanisms of Endotoxin Resistance1986 · 1,281 citations
  4. 4Regulation of the expression of IL-6 in human monocytes.1989 · 170 citations
  5. 5The Saga of Thalidomide1962 · 250 citations