| Autor: |
Dotan I; IBD Service, Dept. of Gastroenterology and Liver Diseases, Tel Aviv Sourasky Medical Center, Tel Aviv 64239, Israel. irisd@tasmc.health.gov.il, Allez M, Nakazawa A, Brimnes J, Schulder-Katz M, Mayer L |
| Jazyk: |
angličtina |
| Zdroj: |
American journal of physiology. Gastrointestinal and liver physiology [Am J Physiol Gastrointest Liver Physiol] 2007 Jun; Vol. 292 (6), pp. G1630-40. Date of Electronic Publication: 2007 Mar 08. |
| DOI: |
10.1152/ajpgi.00294.2006 |
| Abstrakt: |
Previous studies have suggested that intestinal epithelial cells (IECs) have the capacity to function as nonprofessional antigen presenting cells that in the normal state preferentially activate CD8+ T cells. However, under pathological conditions, such as those found in inflammatory bowel disease (IBD), persistent activation of CD4+ T cells is seen. The aim of this study was to determine whether the IBD IECs contribute to CD4+ T cell activation. Freshly isolated human IECs were obtained from surgical specimens of patients with or without IBD and cocultured with autologous or allogeneic peripheral blood T lymphocytes. Cocultures of normal T cells and IECs derived from IBD patients resulted in the preferential activation of CD4+ T cell proliferation that was associated with significant IFN-gamma, but not IL-2, secretion. Cytokine secretion and CD4+ T cell proliferation was inhibited by pretreatment of the IBD IECs with the anti-DR MAb L243. In contrast, normal IECs stimulated the proliferation and cytokine secretion by CD4+ T cells to a significantly lesser degree than IBD IECs. Furthermore, blockade of human leukocyte antigen-DR had a lesser effect in the normal IEC-CD4+ T cell cocultures. We conclude that IECs can contribute to the ongoing CD4+ T cell activation seen in IBD. We suggest that the apparent differences between the secreted levels of IFN-gamma indicate that it may play a dual role in intestinal homeostasis, in which low levels contribute to physiological inflammation whereas higher levels are associated with an uncontrolled inflammatory state. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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