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2004•Humana Press eBooksRequires access

Tumor Necrosis Factor as a Pharmacological Target

Pietro Ghezzi, Anthony Cerami

Open publisher page 25 citations

Abstract

Tumor necrosis factor (TNF) was originally described as a molecule with antitumor properties released by macrophages stimulated with bacterial products. Almost at the same time that TNF was cloned, it was found to be identical to cachectin, a mediator of cachexia. After the finding of this second aspect of TNF action, several studies demonstrated its role as a pro-inflammatory cytokine. These studies led to the use of anti-TNF molecules in rheumatoid arthritis and Crohn's disease. The various strategies used to inhibit TNF are summarized.

About this research paper

What this paper is about

Tumor necrosis factor (TNF) was originally described as a molecule with antitumor properties released by macrophages stimulated with bacterial products. Almost at the same time that TNF was cloned, it was found to be identical to cachectin, a mediator of cachexia. After the finding of this second aspect of TNF action, several studies demonstrated its role as a pro-inflammatory cytokine. These studies led to the use of anti-TNF molecules in rheumatoid arthritis and Crohn's disease. The various strategies used to inhibit TNF are summarized.

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OpenAlex reports 25 citations for this work. Citation counts describe recorded attention and do not establish research quality.

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Available abstract

Tumor necrosis factor (TNF) was originally described as a molecule with antitumor properties released by macrophages stimulated with bacterial products. Almost at the same time that TNF was cloned, it was found to be identical to cachectin, a mediator of cachexia. After the finding of this second aspect of TNF action, several studies demonstrated its role as a pro-inflammatory cytokine. These studies led to the use of anti-TNF molecules in rheumatoid arthritis and Crohn's disease. The various strategies used to inhibit TNF are summarized.

Key concepts: Tumor necrosis factor alpha, Proinflammatory cytokine, Rheumatoid arthritis, Mediator, Cytokine, Cachexia, Immunology, Tumor necrosis factor α

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