Infliximab: Mechanism of action beyond TNF-α neutralization in inflammatory bowel disease
Research output: Contribution to journal › Journal article › Research › peer-review
Treatment of Crohn's disease, a severe chronic intestinal disorder, may at times be challenging as it can be refractory to routine therapy. Among novel therapeutic strategies, agents that neutralize tumour necrosis factor-alpha (TNF-α) are of particular interest because of the crucial role of TNF-α in sustaining chronic mucosal inflammation. The exact mechanism of the anti-TNF action, apart from direct activity that neutralizes cytokines, is not fully understood. Cellular effects of TNF-α neutralizing treatment include an increased susceptibility to apoptosis of intestinal mucosal T cells. A novel pathway of anti-TNF-α interaction with T cells has been presented in the current issue of this journal. Agnholt et al. have found that in-vivo or in-vitro administration of infliximab, a chimeric antibody to TNF-α, resulted in a decreased production of GM-CSF (granulocyte-macrophage colony-stimulating factor) by T cells. Infliximab related down-regulation of TNF-α induced GM-CSF expression may be one of the mechanisms by which this drug increases the rate of apoptosis in T cells.
|Journal||European Journal of Gastroenterology and Hepatology|
|Number of pages||3|
|Publication status||Published - 1 Jul 2004|
- Crohn's disease, Granulocyte-macrophage colony-stimulating factor, Infliximab, T cells