Summary.
The intensive research of recent years has suggested that the cause of ulcerative colitis (UC) involves a genetic predisposition to an uncontrolled or unbalanced immune response to luminal or epithelial antigens or against other external factors. Intercellular adhesion molecule-1 (ICAM-1) is pivotal for the influx of neutrophil granulocytes into colonic mucosa, and gene analyses have found polymorphisms in the gene encoding ICAM-1, indicating that changes in ICAM-1 function may be involved in the pathogenesis of UC. Clinical trials of the ICAM-1 antisense oligonucleotide Alicaforsen, which inhibits the synthesis of ICAM-1, have shown positive results in the treatment of patients with leftsided (distal) UC. In addition to emphasizing the central role of ICAM-1 in active stages of UC, the results provide hope for the development and introduction of a more specific and efficient treatment for UC than those currently available. This review discusses the results from studies on the expression of ICAM-1 in colonic tissue from patients with UC.
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Received 14 March 2005; returned for revision 28 April 2005; accepted by M. J. Parnham 10 May 2005
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Vainer, B. Intercellular adhesion molecule-1 (ICAM-1) in ulcerative colitis: Presence, visualization, and significance. Inflamm. res. 54, 313–327 (2005). https://doi.org/10.1007/s00011-005-1363-8
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DOI: https://doi.org/10.1007/s00011-005-1363-8