Infliximab: Mechanism of action beyond TNF-α neutralization in inflammatory bowel disease
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Infliximab : Mechanism of action beyond TNF-α neutralization in inflammatory bowel disease. / Kirman, Irena; Whelan, Richard L.; Nielsen, Ole H.
In: European Journal of Gastroenterology and Hepatology, Vol. 16, No. 7, 01.07.2004, p. 639-641.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Infliximab
T2 - Mechanism of action beyond TNF-α neutralization in inflammatory bowel disease
AU - Kirman, Irena
AU - Whelan, Richard L.
AU - Nielsen, Ole H.
PY - 2004/7/1
Y1 - 2004/7/1
N2 - 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.
AB - 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.
KW - Crohn's disease
KW - Granulocyte-macrophage colony-stimulating factor
KW - Infliximab
KW - T cells
UR - http://www.scopus.com/inward/record.url?scp=3142559655&partnerID=8YFLogxK
U2 - 10.1097/01.meg.0000108345.41221.c2
DO - 10.1097/01.meg.0000108345.41221.c2
M3 - Journal article
C2 - 15201575
AN - SCOPUS:3142559655
VL - 16
SP - 639
EP - 641
JO - European Journal of Gastroenterology and Hepatology, Supplement
JF - European Journal of Gastroenterology and Hepatology, Supplement
SN - 0954-691X
IS - 7
ER -
ID: 218708396