Expression of adhesion molecules in human intestinal graft‐ versus‐ host disease

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Abstract

The distribution of three cellular adhesion molecules, ICAM‐1. ELAM‐1 and VCAM‐1, was studied in normal rectal mucosa and in graft‐Mrms‐host disease (GvHD) using immunohistological and morphometric techniques. In normal controls, ICAM‐1 was demonstrable on endothelial cells and leucocytes within the lamina propria, ELAM‐I on endothelial cells only and VCAM‐1 on lamina propria leucocytes, many of which exhibited long dendritic processes surrounding the glands. In GvHD, the enterocytes became positive for ICAM‐1 and this was often associated with the presence of intra‐epithelial LFA‐1* lymphocytes and macrophages, ihe latter containing debris of apoptotic cells. The staining was. however, restricted to the luminal membrane of the epithelial cells, raising doubts about the role of ICAM‐1 as a ligand for LFA‐1 on mucosal leucocytes in rectal GvHD. ELAM‐1 expression was increased in GvHD both in terms of the length of positive endothelium and staining intensity. VCAM‐1 was increased on endothelial cells but not leucocytes in the lamina propria in contrast to our previous findings in cutaneous GvHD where VCAM‐+ dendritic cells were increased and endothelial cells remained negative. Normal patterns of adhesion molecule staining were seen in two biopsies exhibiting no morphological evidence of GvHD, from patients who had strong clinical evidence of the disease, indicating that immunostaining for these molecules is unlikely to be of help in improving the sensitivity of histological diagnosis. However, the possibility that adhesion molecule staining may be useful in improving diagnostic specificity by helping to distinguish GvHD from identical histological changes produced by irradiation and cytotoxic drugs is worthy of further investigation. Copyright © 1992, Wiley Blackwell. All rights reserved

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NORTON, J., SLOANE, J. P., AL‐SAFFAR, N., & HASKARD, D. O. (1992). Expression of adhesion molecules in human intestinal graft‐ versus‐ host disease. Clinical & Experimental Immunology, 87(2), 231–236. https://doi.org/10.1111/j.1365-2249.1992.tb02980.x

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