Crohn's disease (CD) is a chronic inflammatory disorder which may involve any part of gastrointestinal tract. Chronic inflammation is primarily due to an immunological imbalance between pro- and anti-inflammatory cytokines, and with a defective apoptosis of lamina propria T cells. Amongst the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) seems to play a central role in pathogenesis of CD. Over the last years, increasing knowledge on the pathogenesis of CD together with progresses in bio-technology have led to the development of a number of biological agents targeting specific molecules involved in gut inflammation, most importantly TNF-α and its receptors. The aim of this paper is to critically review the rationale and state-of-the art for the TNF- α inhibitors in the treatment of CD.

Crohn's disease (CD) is a chronic inflammatory disorder which may involve any part of gastrointestinal tract. Chronic inflammation is primarily due to an immunological imbalance between pro- and anti -inflammatory cytokines, and with a defective apoptosis of lamina propria T cells. Amongst the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) seems to play a central role in pathogenesis of CD. Over the last years, increasing knowledge on the pathogenesis of CD together with progresses in bio-technology have led to the development of a number of biological agents targeting specific molecules involved in gut inflammation, most importantly TNF-alpha and its receptors. The aim of this paper is to critically review the rationale and state-of-the art for the use TNF-alpha inhibitors in the treatment of CD.

Tumor necrosis factor-alpha monoclonal antibodies for Crohn's disease: Tipping the balance

Danese S;Repici A;Malesci A
2007-01-01

Abstract

Crohn's disease (CD) is a chronic inflammatory disorder which may involve any part of gastrointestinal tract. Chronic inflammation is primarily due to an immunological imbalance between pro- and anti-inflammatory cytokines, and with a defective apoptosis of lamina propria T cells. Amongst the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) seems to play a central role in pathogenesis of CD. Over the last years, increasing knowledge on the pathogenesis of CD together with progresses in bio-technology have led to the development of a number of biological agents targeting specific molecules involved in gut inflammation, most importantly TNF-α and its receptors. The aim of this paper is to critically review the rationale and state-of-the art for the TNF- α inhibitors in the treatment of CD.
2007
Crohn's disease (CD) is a chronic inflammatory disorder which may involve any part of gastrointestinal tract. Chronic inflammation is primarily due to an immunological imbalance between pro- and anti -inflammatory cytokines, and with a defective apoptosis of lamina propria T cells. Amongst the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) seems to play a central role in pathogenesis of CD. Over the last years, increasing knowledge on the pathogenesis of CD together with progresses in bio-technology have led to the development of a number of biological agents targeting specific molecules involved in gut inflammation, most importantly TNF-alpha and its receptors. The aim of this paper is to critically review the rationale and state-of-the art for the use TNF-alpha inhibitors in the treatment of CD.
inflammatory-bowel-disease; placebo-controlled trial; caspase-dependent pathway; endothelial growth-factor; transmembrane TNF-alpha; propria T-lymphocytes; NF-kappa-B; double-blind; rheumatoid-arthritis; intestinal inflammation
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11699/3161
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