Abstract
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.
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | European Journal of Gastroenterology and Hepatology |
| Vol/bind | 16 |
| Udgave nummer | 7 |
| Sider (fra-til) | 639-641 |
| Antal sider | 3 |
| ISSN | 0954-691X |
| DOI | |
| Status | Udgivet - 1 jul. 2004 |